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advancements in pro-aging







Dear Colleagues and health professionals, Welcome to the Lifespan Medicine Magazine (LSMM). The LSMM is an internet magazine that aims to provide health professionals with cutting-edge and information concerning all therapies that may not only help to prevent or slow down aging, but also to help reverse it in order that human beings may live long and healthy lives. This magazine is oriented to provide positive, practical and scientific information… a step further than ‘antiaging medicine’. We believe that the best way to advance in age is to try continuously to become healthier all the time and to focus on reversing aging rather than ‘merely’ stopping aging or slowing it down. Additionally, we want to present the best educational or training programs for physicians who want to improve their skills in lifespan medicine. You need and deserve the best. The more skilled you become, the better your patients will be treated and we hope that the LSMM will be your window into those goals.

Index 3

Index and Introduction from Dr. Thierry Hertoghe

4 -7

Oxytocin and autism

We intend to start with a publication every 6 months, but consider more frequent editions if there is interest to do so. So please do not hesitate to provide us your feedback and comments as we will use them to build a better Lifespan Medicine Magazine for you.

9 - 11

Melatonin ARMD

12 - 14

Balancing thyroid activity

16 - 19

Urinary Organic Metabolites


Carbs’ Surprising Heart Disease Connection

I’m hoping to hear from you soon,

22 - 24

The Multivitamin

Thierry Hertoghe


Lutein slows vision loss

27 - 29

Italian Secrets

Dr. Thierry Hertoghe

30 - 35

The age of antibiotics may be coming to an end- what can we turn to?

Our initial aim is to start with written texts (with references naturally) and later to add video presentations too.

President of the World society of Anti-Aging Medicine President of the International Hormone Society

The Lifespan Medicine Magazine Editor in Chief: Thierry Hertoghe, M.D. Assistant Editor: Phil Micans, MS, PharmB To join our mailing list, or to send us comments about the magazine and features you would like to see in it, please email us at: (please note we will not answer or give medical advice). Disclaimer: All information contained within is educational and is not intended to replace the advice of a physician. Any claims, opinions, statements or references contained within are not necessarily the same as those of the LSMM and cannot be guaranteed as accurate. All copyrights are acknowledged and whist every effort has been made to ensure accuracy, no responsibility can be accepted for illustrations, photographs, artwork or advertising materials while in transmission or with the publisher or their agents.


Oxytocin and autism Oxytocin: Relief for autism in children, schizophrenia in adults and the progressively lower sociability appearing in elderly people? By Dr. Thierry Hertoghe, President of the International Hormone Society and author of the bestselling ‘Hormone handbook’ for physicians and ‘Patient Hormone Handbook’ Great enthusiasm has emerged in part of the general public and medical community for the beneficial effects of hormone therapies to counter or even reverse aging. Among all those endocrine treatments, one emerges as a major tool to counter emotional aging, in particular the progressive loss of interest and happy feelings in social encounters people may experience when they age. With aging, more and more people feel the presence of others as more disturbing and unpleasant than before. Consequently, they increasingly tend to isolate themselves from others. They start developing ‘schizophrenic traits’. A growing number of publications suggest that oxytocin therapy may relief such pathological traits.1 To understand this better; let’s review the incidence of oxytocin deficiency in autism and schizophrenia, the two diseases that make people isolate themselves from others, and the potential help that oxytocin therapy may deliver to help solve these disturbing diseases.

Low oxytocin in autism In autism, children tend to stay alone, socially isolated from others, as though living in another world. They are not attracted to others. They feel cool or cold inside, not emotionally warm enough to go and meet other people. In reality, many children with autism stay active all the time, filling up the emptiness and coldness of their world with 4

activity, showing repeated stereotype behavior, as if repetitive movements could warm up their cold world. Young children, for example, may loadblocks one upon the other and then when the whole pack falls apart, start over again, piling up one block above the other. As autistic children have few and poor contacts with other kids and adults, they live in a world of their own with its own rules and language. They may utter strange words and sentences invented by them, words that have no meaning for outsiders. The typical autistic tendency to lower sociability is found in people with low oxytocin too.1 Does this mean that oxytocin deficiency might cause some, and perhaps many, of the symptoms of autism? What does research reveal? A series of studies demonstrate that oxytocin deficiency is closely related to autism. For example, autistic children have lower levels of oxytocin. Worse, the relative oxytocin deficiency is aggravated by the presence of higher levels of inactive oxytocin precursors, oxytocin combined to amino acids that may block oxytocin receptors.2 Moreover,, when autistic children become adolescents, the level of oxytocin remains low in the blood just as in childhood, while in normal adolescents it substantially increases at that time, predicting an aggravation of the oxytocin deficiency in adolescence.3 Last but not least, disturbing evidence shows that the oxytocin deficiency in autism is in fact worse than was expected, based on blood values. Researchers have discovered that in autism a genetic abnormality may aggravate the oxytocin deficiency. Oxytocin receptors in the cells may be abnormal and poorly responsive to oxytocin action, an effect that partially blocks oxytocin action.4

Oxytocin to treat autism Administered to animals, oxytocin increases the frequency of social contacts between animals. To do so, it must increase the desire and ability to come into contact with others of the same species and become attached to them, features that are virtually absent in autistic children. Some isolated studies in humans have indicated that oxytocin administration may help autistic children to be more socially involved. Oxytocin may correct or at least improve social binding, but the duration of

the experiences with oxytocin are generally too short (often one-day- or one-week experiences) to obtain any major effect or conclusive evidence.

The fascinating autistic experience in rats A fascinating experiment in rats has raised the hope that oxytocin could be the cure, or at least an aid for autism. Researchers made rats autistic by stressing them, while they still were in the mother’s womb.6 In order to put the rats under intense stress before birth the researchrs created constant worries in the pregnant mother rat during the last week of the pregnancy, an experience that in humans would be equivalent to stressing a woman during the two last months of her pregnancy. Young rat pups became ‘autistic’ after delivery. They came about six to eight times less frequently into contact with other ‘normal’ rat pups (who were not stressed during pregnancy). In addition, whenever - in rare occasions - the autistic rats met other rats, the contacts were of lower quality and intensity than those that occurred between normal pups. After growing up into adults, the autistic rats continued to show the same poor social behavior. When researchers added oxytocin to the drinking water of the grownup adult autistic (or schizophrenic) rats, their surprise was great. The dull and asocial animals became as sociable as normal rats. The rats initiated social contacts as often as never-stressed rats. The quality and intensity of these new social contacts were also as good as in normal rats (see figure 4).5

Figure 4: Oxytocin treatment of adult rats, which were heavily stressed in utero before birth, completely reverses their schizophrenic low sociability and increased 8-fold the number of social contacts with other rats.

The success of oxytocin in animal autism makes us wonder whether oxytocin could cure human autism. At present, trials in children are ongoing and preliminary results are awaited.

Low oxytocin in schizophrenia In schizophrenia, the adult form of autism, oxytocin deficiency may be rampant too. For example, schizophrenic patients who tend to drink large amounts of water have lower levels of oxytocin.6 Why would oxytocin levels be lower in patients who drink abnormal amounts of water? Maybe because these patients with schizophrenia have, next to a defiency in oxytocin, also a deficit in vasopressin, a hormone that is produced in the same brain tissues as oxytocin. Vasopressin also improves social contacts, although to a lesser degree than oxytocin. Vasopressin’s main role is to keep water in the body. Vasopressin deficiency causes increased water loss in the urines, also called diabetes insipidus. Diabetes insipidus produces a terrible thirst, making patients drink copious amounts of water or other fluids throughout the day, and, consequently, go to the toilet all the time to urinate large volumes of almost transparent urine. Urination is most spectacular at night where the patients have to go two to six times to the toilet pouring out large volumes of urine. A combination of oxytocin and vasopressin deficiencies is in most cases caused by malfunction of the parvoventricular and supraoptic nuclei in the hypothalamus, where both hormones are produced, or in some cases by weakness of the pituitary gland, where both hormones are released into the bloodstream. Patients with schizophrenia experience in general great difficulties to behave and feel well when they meet other people. A study showed that this social maladaption may also be due to a failure in their oxytocin production. When healthy people were placed in an experimental situation where they met other people they had to trust, their blood level of the hormone of trust oxytocin clearly rose. In contrast, placed in the same situation schizophrenic patients showed no or weak oxytocin level elevations, possibly indicating that they didn’t or couldn’t really trust the other people. Worse even, in many patients with schizophrenia 5

the oxytocin levels even dropped during their meeting with other people, the opposite of what happened in normal people. When oxytocin levels drop, the patients may react with typical ‘negative’ symptoms of schizophrenia such as withdrawal from the interaction and isolation.7 Further evidence in support of the existence of oxytocin deficiency in schizophrenic adults comes from the discovery of an impairment of oxytocin neurotransmission. In essence the tissues in their brain respond less to oxytocin.8

Oxytocin reduces schizophrenic symptoms Oxytocin has been administered to schizophrenic adult patients. Results are promising, but not yet entirely convincing, probably because of the (too) short duration of the studies. Schizophrenic patients are characterized by social maladjustment, emotional inabilities and rigid stereotype behaviors - such as repeatedly washing the hands 15 times a day. In two of these experiments, oxytocin improved two of the three major impairments for schizophrenic adults. In one trial, oxytocin helped the patients to better recognize emotions in speech, something these patients are often unable to do. Helped by oxytocin, the patients became increasingly more able to distinguish between happy, indifferent, angry and sad feelings in a speech.9 In a further investigation, oxytocin reduced their typical repeated stereotype behaviors such as the repetitive washing of the hands.10 Thus, short term administration of oxytocin can reduce behavioral deviations of schizophrenia. However, to improve sociability more in schizophrenic patients who are deeply social maladjusted, prolonged uses of oxytocin, beyond the one or two weeks of the actual timid trials, might be necessary. This is my experience that I have noted with less afflicted patients. Researchers should be encouraged to make longer trials of three months to one year duration. Such trials are likely to achieve greater results that would justify the inclusion of oxytocin as a treatment for autism and schizophrenia. In the meantime, considering the great safety of oxytocin, low doses of sublingual oxytocin between 2.5 and 10 to 15 international units per 6

day, possibly up to 50 international units per day in more resisting cases, should be tried to relieve patients from their sufferance.

Oxytocin improves contacts with other people With age, most people become less sociable. This may be caused by a progressive decline in oxytocin. Indeed, our ability and desire to live in families, work with others in offices or workplaces, go shopping together, drive in a car together, or go to conferences where many people gather, is mainly due to the action of one hormone in our blood: oxytocin. Oxytocin adds pleasure. It makes contacts with family members and other people for us more pleasant and enjoyable. It makes us want to meet them, stay in groups and go to parties full of people. Without oxytocin we would prefer to stay at home alone, sheltered away from the other humans who we would find uninteresting. We would be schizophrenics, people who come only into contact, and then briefly, with others for essential activities such as finding food, water and a shelter or home. Without oxytocin, we would tend to avoid any contact with others that would not be essential for survival. You and I would be loners, remote people with poor pleasure in life, especially in activities that involve other people. Research has confirmed the link between oxytocin and sociability.11-14 Breastfeeding women who have a lower level of oxytocin, for example, report being less sociable and more lonely.15

Attachment with Oxytocin With age, people often feel more detached from others, more neutral, as if their capacity to love others has decreased. Can oxytocin deficiency explain this loss of attachment? It is likely. A major effect of oxytocin is its capacity to make you feel warmly attached to people and groups of persons who bring security and stability such as the family. Oxytocin is the attachment hormone. The higher the level of

oxytocin is in people the easier and more intense they attach themselves to others. Oxytocin increases attachment by appeasing the anxiety for encounters with other individuals, while it increases at the same time the pleasure and excitement we feel for them. People who are rich in oxytocin see their family members and friends with great pleasure, a lot of fun and full of warmheartedness. 16-18 In one experiment, young men were asked to take oxytocin and then to view pictures of different conditions. The intake of oxytocin enhanced the men’s preference for pictures that evoked attachment - further evidence that oxytocin works well to boost attachment.18 Thus, an increasingly greater number of scientific data supports the view that oxytocin should be incorporated into typical hormone treatments that help prevent, slow down or even reverse aging. In my experience as a physician working in this field possibly one third of patients require and may respond well to such a treatment with great safety margin.

References: 1. Passion, sex and long life, the incredible oxytocin adventure? Hertoghe T., International medical books, Luxemburg, 2010,

Oxytocin: a relief for autism and schizophrenia? 2. Uvnäs-Moberg K. Neuroendocrinology of the motherchild interaction. Trends Endocrinol Metab. 1996 MayJun;7(4):126-31. 3. Green L, Fein D, Modahl C, Feinstein C, Waterhouse L, Morris M. Oxytocin and autistic disorder: alterations in peptide forms. Biol Psychiatry. 2001 Oct 15;50(8):609-13. 4. Modahl C, Green L, Fein D, Morris M, Waterhouse L, Feinstein C, Levin H.Plasma oxytocin levels in autistic children. Biol Psychiatry. 1998 Feb 15;43(4):270-7. 5. Bornstein G, Knafo A, Yirmiya N, Ebstein RP. Molecular genetic studies of the arginine vasopressin 1a receptor (AVPR1a) and the oxytocin receptor (OXTR) in human behaviour: from autism to altruism with some notes in between. Prog Brain Res. 2008;170:435-49

with neuroendocrine dysfunction and emotional deficits. Schizophr Res. 2008 Jan;98(1-3):247-55. 8. Kéri S, Kiss I, Kelemen O. Sharing secrets: oxytocin and trust in schizophrenia. Soc Neurosci. 2009;4(4):287-93. 9. Mai JK, et al.Morphometric evaluation of neurophysinimmunoreactivity in the human brain: pronounced interindividual variability and evidence for altered staining patterns in schizophrenia. J Hirnforsch. 1993;34:133–154 10. Hollander E, Bartz J, Chaplin W, Phillips A, Sumner J, Soorya L, Anagnostou E,Wasserman S.Oxytocin increases retention of social cognition in autism.Biol Psychiatry. 2007 Feb 15;61(4):498-503. 11. Hollander E, Novotny S, Hanratty M, Yaffe R, DeCaria CM, Aronowitz BR, Mosovich S.Oxytocin infusion reduces repetitive behaviors in adults with autistic and Asperger’s disorders. Neuropsychopharmacology. 2003 Jan;28(1):193-8.

Oxytocin improves contacts with other people 12. Fries AB, Ziegler TE, Kurian JR, Jacoris S, Pollak SD. Early experience in humans is associated with changes in neuropeptides critical for regulating social behavior. Proc Natl Acad Sci U S A. 2005;102:17237–40 13. Insel TR. A neurobiological basis of social attachment. Am J Psychiatry. 1997;154:726–35. 14. Lee PR, Brady D, Shapiro RA, Dorsa DM, Koenig JI. Social interaction deficits caused by chronic phencyclidine administration are reversed by oxytocin Neuropsychopharmacology 2005. 30:1883–94 15. Young LJ. Frank A. Beach Award. Oxytocin and vasopressin receptors and species-typical social behaviors. Horm Behav. 1999;36:212–21. 16. Uvnäs-Moberg K. Neuroendocrinology of the motherchild interaction. Trends Endocrinol Metab. 1996 MayJun;7(4):126-31.

Attachment with Oxytocin 17. Tops M, van Peer JM, Korf J, Wijers AA, Tucker DM. Anxiety, cortisol, and attachment predict plasma oxytocin. Psychophysiology. 2007 May;44(3):444-9. 18. Insel TR. A neurobiological basis of social attachment. Am J Psychiatry. 1997;154:726–735. 19. Buchheim A, Heinrichs M, George C, Pokorny D, Koops E, Henningsen P, O’Connor MF, Gündel H. Oxytocin enhances the experience of attachment security. Psychoneuroendocrinology. 2009 Oct;34(9):1417-22

6. Lee PR, Brady DL, Shapiro RA, Dorsa DM, Koenig JI. Prenatal stress generates deficits in rat social behavior: Reversal by oxytocin. Brain Res. 2007 Jul 2;1156:152-67 7. Goldman M, Marlow-O’Connor M, Torres I, Carter CS. Diminished plasma oxytocin in schizophrenic patients



Melatonin ‘&’ ARMD

Study highlights that melatonin, zinc and selenium can improve both wet and dry forms of age related macular degeneration

such as reading or driving very difficult. A test to determine the presence of ARMD uses something called an Asmler grid. This involves starring at a center dot to see if the lines around it are affected by blurriness, waviness or even are out of vision altogether.

By Phil Micans, MS, PharmB, International Antiaging Systems

ARMD background

Age-related macular degeneration (ARMD) is the leading cause of severe visual loss in older people, indeed it is the main cause of central vision loss (blindness) in the USA today for those over the age of fifty; (Source: American Academy of Ophthalmology). Macular degeneration is a condition whereby the light sensing cells in the eye’s macula malfunction and eventually they cease to work. Often individuals with macular degeneration will notice that straight lines, such as poles, walls or wires appear to be wavy; other symptoms can include blurred text, often with dark or even empty spaces that may block the center of the field of vision. Fortunately, macular degeneration rarely results in complete blindness since side vision is usually unaffected, but even so because of its propensity, it has been estimated that more than a million people worldwide are completely blind because of advanced ARMD. ARMD makes activities that require sharp vision

It is not clear how or why ARMD is triggered, although the main focus has been on the hardening of arteries that supply the retina at the back of the eye. Over time this deprives the tissues of oxygen and other nutrients that help it to protect itself and to thrive, the consequence of which is a gradual deterioration of vision. The central part of the retina contains a yellow pigment called macular pigment, this helps to protect the receptors in the retina from sunlight, especially from the harmful effects of blue light. The lessening of the density of this protective pigment can be linked to poor diet and in those who smoke, thus its protection from free radical damage and its enrichment are also seen as a key to ARMD. Physicians classify ARMD into two parts, namely wet and dry. The wet form affects about 15% of patients with ARMD. This form differs from the dry type in that there is a growth of abnormal blood vessels under the retina. This can lead to bleeding and scarring and results in a more rapid and severe progression 9

of the disease (when compared to the dry form). Luckily for about 70% of patients with the wet form of ARMD they can be treated with laser photocoagulation to help stabilize the vision, or to limit the growth of further abnormal blood vessels. So whilst the dry form affects 85% of patients with ARMD and thankfully is less progressive and not as severe as the wet form, unfortunately to-date there have been no successfully reported treatments in regard to the reversal of this condition. Presently most treatments for all ARMD’s have relied heavily upon supplementing with nutritional elements, particularly lutein and zeaxanthin to alleviate, slow down and sometimes halt its progression.

The study reported that at 2-3 months of treatment the visual acuity had been kept stable, (in other words there appeared to be a halting of the progression of ARMD in general). It is worth noting that although this follow up time is not long, this result is already better than the otherwise normal course that could be expected. For the patients who continued onward past 6 months and onto 12 months of nightly use of 3 mg of melatonin combined with 50 mg of zinc orotate and 50 mcg of selenium (in a formula known as Melatonin Zn Se®) saw a change in their Fundus pictures that were remarkable, (please note the before-and-after eye pictures presented within this article in figures 1-3).

A breakthrough for ARMD? Now a new study; (Changxian Yi et al, effects of melatonin in age-related macular degeneration, Ann NY Acad Sci, 1057:384-392) gives hope to millions with ARMD. Dr. Changxian Yi studied 100 patients over a period of 2-years to see if treatment with tablets of Melatonin Zn Se ® (so called because it also contains zinc and selenium in addition to melatonin), could help the condition of ARMD. His thinking was that melatonin could have the capacity to control eye pigmentation and thereby regulate the amount of light reaching the photoreceptors. The unique combination in the tablets could also scavenge hydroxyradicals and help to protect retinal pigment epithelium cells from oxidative/ free radical damage- knowing that this damage is also considered to be a cause for the initiation of ARMD. As Dr. Changxian stated; “Our purpose was to explore a new approach to prevent or treat ARMD.” The approach was very simple; firstly the patients were diagnosed with ARMD, with both the wet and dry forms included. Then 3 mg of Melatonin Zn Se were given orally each night at bedtime for a minimum of 3 months, with 55 patients continuing on for more than 6 months and some onto 12 and 24 months. The patients were then evaluated at regular periods to measure the extent of their ARMD.


Figure 1: The left slide shows the eye of a 67 year old male before treatment, his vision had been deteriorating for 2-years. The right picture shows the same eye 2-months later after daily ingestion of a Melatonin Zn Se® tablet. He now has stable visual acuity of 0.3 with remarkable improvements in sub-retinal macular haemorrhage.


Figure 2: The left slide shows the eye of a 71-year old female with ARMD who after 6-months of a Melatonin Zn Se® tablet daily had her vision improve from 0.2 to 0.4 (as indicated in the right slide).

Figure 3: A 58 year old male whose visual acuity at the start (left slide) was 0.2. This improved to 0.4 after 6-months of regular use of a Melatonin Zn Se® tablet. The sub-retinal haemorrhage and exudates were remarkably absorbed.

At the end of the study, of the original 110 eyes tested only 8 eyes showed more retinal bleeding and 6 eyes more retinal exudates, the vast majority had dramatically reduced pathologic macular changes. This was made self-evident by the patients themselves reporting better vision and general ocular experience with improvements to flare, dryness, clarity and comfort. Whilst the authors called for larger studies to confirm their findings, they concluded that; “melatonin supplementation among the aged population may be beneficial in preventing, relieving or reducing the severity of ARMD, which is one of the leading causes of blindness in the elderly.” What’s more during the entire period, (with some patients taking the 3mg tablets every night for 2-years) no significant side effects were observed.

Dr. Pierpaoli’s views We spoke with world melatonin expert Walter Pierpaoli, M.D., author of the bestselling melatonin books; the melatonin miracle and the key of life about this new finding, he told us; “Many people are aware of melatonin’s role in jet-lag, or as a potent antioxidant, but we know it is far more than this. Our research with melatonin has highlighted its ability to re-synchronize the endocrine system as well as the circadian rhythms of the wake-sleep cycles. I note that whilst the authors of the ARMD study have discussed the role of melatonin in the eye as being able to control eye pigmentation, to help regulate the amount of light reaching the photoreceptors and other functions in relation to eye structure as possible factors in the benefits for ARMD; I also surmise that through the rebalancing of hormones and improvement of repair functionsthrough better sleep patterns- that these have also had this significant and profound ability to reverse this condition.”

is one of those molecules that existed before life began and that it has been put to a special use.” Asked whether there may be further studies regarding ARMD and melatonin, Dr. Pierpaoli said; “We accept that additional studies are needed to confirm these results and its mechanism, however we are delighted that a vital benefit to slow, halt and even reverse ARMD has been discovered. Whatever the outcome of further research into the pathways and actions of the Melatonin Zn Se, the fact remains that thousands, even millions of people can now benefit from this research to protect their vision.” As one of the world’s leading antiaging researchers, Dr. Pierpaoli has been exposing the benefits of his own and others work with melatonin, particularly at the unique bi-annual Stromboli conference in Italy (see for details). When asked for a final comment on the ARMD findings he said; “Here is yet another clinical study, this time about age-related macular degeneration, that can be added to the long list of disorders that include cancer, Alzheimer’s, cardiovascular, depression and even aging itself, all of which can be successfully ameliorated with Melatonin Zn Se®.”

Dr. Pierpaoli went on to say; “We’ve seen many miraculous reversals of diseases in our patients with Melatonin Zn Se®, this latest study showing that it can halt and even reverse age-related macular degeneration is another important highlight of its power.” In the past Dr. Pierpaoli has gone on record to say that melatonin is a very unique molecule, going as far as to announce that; “In my opinion melatonin


Balancing Thyroid Activity Nutritionals therapies to better balance thyroid activity In order to achieve optimal function and to produce thyroid hormones in sufficient quantities to respond to the body’s needs, the thyroid uses a certain number of nutrients, including minerals such as iodine, magnesium, selenium and zinc, the B-group Vitamins and the amino acid L-Tyrosine. Research has also shown that forskolin or guggulsterones may improve thyroid activity, whilst also promoting weight loss.

The thyroid gland plays an important controlling role in the metabolic activity of practically every tissue in the body. It secretes hormones which are indispensible to health on many levels. A wellbalanced thyroid gland is one of the keys to the prevention of aging. It also allows better weight control. Thyroid hormones include T4 (thyroxin or tetraiodothyronine), T3 (triodothyronine), reverse T3 (rT3), and, in very small quantities, T2 (diiodothyrosine) and T1 (mono-iodothyrosine). A healthy thyroid secretes around 80mcg a day of T4; 4 mcg of T3 and 2mcg of rT3. T3 is the most active form, rT3 is relatively inactive. In the other tissues of the body, T4 is converted into T3 and rT3, supplementing the small amounts secreted by the thyroid. Differing only in the number of iodide atoms that they contain, these hormones have the same organic structure, iodothyronine, derived from tyrosine, an amino acid.

Age-related changes in thyroid function As we age, thyroid function weakens. As levels of T3 and T4 decline, those of TSH (thyroid stimulating hormone) rise slightly. However, although there is an increase in symptoms linked to hypothyroidism in the older population, changes in the levels of these hormones in the blood are often much less 12

significant than the severity of the symptoms would lead you to suppose. One of the reasons for this apparent stability in the blood levels of T3 and T4 (in spite of the reduction in T4 production by the thyroid) is that the metabolic degradation of these hormones diminishes, allowing the blood concentrations to remain unchanged. A study published in the British Medical Journal shows that out of 80 patients with a diagnosis of hypothyroidism, based on clinical symptoms, only five of these had abnormally low T4 levels, alongside elevated TSH levels.

L-Tyrosine, a biologic precursor of thyroid hormones L-Tyrosine, an essential amino acid, is used, alongside iodine, to produce thyroid hormones of which it is the biological precursor. Important to the structure of almost every protein in the body, L-Tyrosine binds itself to iodine atoms to create the thyroid hormone. The body produces L-Tyrosine naturally from other amino acids. But, over time, this production reduces and becomes insufficient to respond to the needs of the thyroid. Supplementation is therefore important to maintain normal function.

Iodine, indispensable to the production of thyroid hormones The body needs iodine to produce thyroid hormones. Small to moderate iodine deficiencies may lead to the development of a goitre (an abnormal swelling of the thyroid gland). The thyroid is the only part of the body capable of capturing and retaining iodine. It is an essential component of the T3 and T4 hormones. In order to respond to the body’s needs for thyroid hormones, the thyroid extracts iodine from the blood and incorporates it into the thyroid hormones. Other minerals, including iron and zinc are essential to the normal metabolism of thyroid hormones. Any deficiencies in these elements can disturb thyroid function.

Zinc, and selenium, vital to thyroid function Zinc boosts thyroid function. Its levels are generally high in cases of hyperthyroidism and

low in cases of hypothyroidism. In animal studies, deficiencies in zinc, selenium and/or iodine have shown distinct effects on the metabolism and structure of the thyroid. Zinc deficiency has been linked to around a 30% reduction in serum T3 concentration and in free thyroxin compared to controls with normal zinc status. In patients with low levels of T3, zinc can play a role in the metabolism of thyroid hormones and could contribute to the conversion of T4 into T3i. This effect has been confirmed by a study carried out on schoolgirls deficient in zincii.

week training programme. Two groups (one for the sedentary subjects and the other of subjects practicing 90 to 120 minutes of taekwondo five days a week) received 10 mg of magnesium per day, per kilogram of body weight. A third group undertook physical exercise without being given supplemental magnesium. The results showed that physical exercise to the point of exhaustion provoked a reduction in thyroid activity in both the sedentary individuals and the trained athletes and that supplementation with magnesium prevented this reduction in activity. vii

Selenium is more concentrated in the thyroid gland than in any other organ, which suggests its importance to the normal functioning of the thyroid. It acts as an antioxidant, protecting the thyroid gland, as well as a cofactor facilitating the production of thyroid hormones and promoting the conversion of T4 into T3.

Thyroid function affects Vitamin B levels

The thyroid enzyme peroxidase (TPO) facilitates the binding of iodine with tyrosine to form the thyroid hormone. Normal TPO activity generates a great number of free radicals in the thyroid gland in the form of H2O2 and lipid peroxides. These must be deactivated by selenium-dependent enzymes to ensure that the production of thyroid hormones is not disrupted and the thyroid gland does not become inflamed. Selenium is a component of the type I 5’deiodinase enzyme, which helps to convert T4 into T3 in peripheral tissues. A selenium deficiency could therefore disrupt thyroid function and lead to hypothyroidism.iii A study carried out on 109 euthyroid subjects (those with normal thyroid function) indicated that the decline in T4 to T3 conversion in the peripheral tissues is linked, in the older generation, to insufficient selenium levels.iv Researchers also believe that a selenium deficiency can aggravate the effects of iodine deficiency on thyroid function and that suitable levels of nutritional selenium can help to protect against certain of its neurological effects.v vi

In subjects with hypothyroidism, folic acid levels appear to be reduced.viii In addition, serum concentrations of homocysteine are more elevated in women with hyperactive thyroids than in those with normal thyroid function. A study carried out on 50 underactive thyroid patients and 46 hyperactive thyroid patients showed that folate levels were lower in those with hypothyroidism and higher in those with hyperthyroidismix. Another study examined 31 young women with hypothyroidism and 30 young women in good health and evaluated their total plasma concentrations of homocysteine, folate and cobalamine before and after treatment with L-thyroxine. The treatment lowered homocysteine levels, but had no effect on folate or cobalamine levels.x

Forskolin activates adenylate cyclase Forskolin is extracted from the Coleus forskohlii plant, traditionally used in Ayurvedic medicine to treat a great number of health problems including asthma, hypertension, eczema, psoriasis and cardiac insufficiency.

Magnesium prevents a reduction in thyroid activity

Forskolin acts primarily to activate the adenylate cyclise enzyme, thus increasing cyclic adenosine monophosphate (cAMP) in the cells. cAMP belongs to a class of substances known as “secondary messengers”. Increasing cellular cAMP brings with it a great number of physiological and biochemical effects, in particular an increase in thyroid function.

A study examined the effect of magnesium on the thyroid hormones of both sedentary subjects and subjects practicing taekwondo during a four-

Forskolin has demonstrated its ability to increase thyroid hormone production and to stimulate their release. This thyroid stimulation mechanism


supports metabolism and could be one of the mechanisms by which forskolin promotes weight loss. Its normalising action on thyroid function may also contribute to its antidepressant effect, depression being one of the well-known characteristics of hypothyroidism.

Guggulsterones stimulate the thyroid and promote weight loss Guggulsterones, extracted from Commiphora mukul, have been used in Ayurvedic medicine for thousands of years to treat arthritis, inflammation, bone fractures, obesity or lipid metabolism problems. Guggulsterones have been identified as promoting weight loss. They activate the lipolytic enzymes and increase T3 levels, probably by increasing the conversion in the liver of T4 into T3 and by directly stimulating the thyroid gland.xi Their ability to stimulate the thyroid gland could in part explain how they can act on cholesterol levels and promote weight loss by increasing the body’s metabolism. Administered to albino rats (1 g per 100g of body weight), guggulsterones provoked an increase in iodine consumption by the thyroid and stimulated thyroid peroxidase and protease activity, as well as oxygen consumption by isolated sections of the liver and bicep muscles.xii Studies have shown that they are able to increase blood concentrations of thyroid hormone. In particular, they elevate the ratio of T3 to T4. At the same time, a reduction in the normal oxidative lesions on the liver is observed. This observation is particularly interesting, given that the liver is the primary site for T4 storage and for T3 regeneration. Once thyroid activity has been stimulated and metabolic rhythm has been restored to normal, weight loss may happen more easily and rapidly. Several subjects followed a weight loss program for six weeks involving diet, physical exercise and, for a selection of them, the taking of a nutritional supplement containing guggulsterones. The subjects taking the guggulsterones lost close to 5kg of fat in comparison to the 1.5kg lost by those not supplemented. At the same time, when thyroid activity was measured in a few of the 14

subjects, they found an 8-10% increase in thyroid hormone levels.

References: i.

Nishiyama S. et al., Zinc supplementation alters thyroid hormone metabolism in disabled patients with zinc deficiency. J. M. Coll. Nutr., 1994 Feb., 13:62-7.

ii. Maxwell C. et al., Effect of zinc supplementation on thyroid hormone function. A case study of two college females, Ann. Nutr. Met., 2007, 51(2):188-94, e-pub 2007 May 30 iii. Wu H.Y. et al., Selenium deficiency and thyroid hormone metabolism and function, Sheng Li Ko Hsueh Chin Chan, 1995 Jan, 26(1):12-6 iv. Olivieri O. et al., Selenium, zinc and thyroid hormones in healthy subjects : low T3/T4 ratio in the elderly is related to impaired selenium status, Biol. Trace Elem. Res., 1996 Jan, 51(1):31-4 v. Arthur J.R., The role of selenium in thyroid hormone metabolism, Can. J. Physiol. Pharmacol., 1991, 69:164852 vi. Corvilain B. et al., Selenium and thyroid : how the relationship was established, Am. J. Clinical Nutr., 1993, 57 (2 suppl) : 244S-8S vii. Cinar V., The effects of magnesium supplementation on thyroid hormones of sedentars and Tae-KwonDo sportperson at resting and exhaustion, Neuro Endocrinol. Lett., 2007 Oct, 28(5):708-12 viii. Lindenbaum F. et al., Folic acid clearances and basal serum folate levels in patients with thyroid disease, J. Clin. Pathol., 1964 Nov, 17(6):666-670 ix. Diekman M.J. et al., Determinants of changes in plasma homocysteine in hyperthyroidism and hypothyroidism, Clin. Endocrinol., Oxf., 2001 Feb, 54(2):197-204 x. Orzechowska-Pawilojc A. et al., Homocystein, folate and cobalamin levels in hypothyroid women before and after treatment. xi. Panda S. et al., Gugulu (Commiphora mukul) induces triiodothyronine production : possible involvement of lipid peroxidation, Life Scien., 1999, 65(12) :PL137-41 xii. Tripathi Y.B. et al., Thyroid stimulating action of Z-guggulsterone obtained from Commiphora mukul, Planta Med., 1984 Feb, 50(1):78-80 xiii. Antonio J. et al., Effects of a standardized guggulsterone phosphate supplement on body composition in overweight adults : a pilot study, Current Therapeutic Research Clinical and Experimental, 1999, 60:2220-227

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Urinary Organic Metabolites By: Dr Georges Mouton, MD, Functional Medicine


rats from group “B” were excreting predominantly hippuric acid (HA)2 (fig.1):

In 1994 already, studies of human clinical samples showed that gas chromatography/ mass spectrometry (GC-MS) techniques have a “potential for diagnosis and studies of metabolism in situ”1. Researchers found that, when this technique is applied to blood or urine, information can be gathered on the infected host microbial metabolism 1. A more recent study (2002), published in Xenobiotic, provided convincing evidence that the level of several urinary organic metabolites can be affected by differences in the metabolic capability of the intestinal microflora2.

Central Toxicology Laboratory Animal Study This animal study took place in Macclesfield (UK) at the Central Toxicology Laboratory (CTL) in Alderley Park. The sample was constituted of two groups of rats of an identical genetic lineage. To prevent any bacterial cross-contamination, the two groups of rats were housed under the same environmental conditions on two different floors of a barriered breeding unit, both groups being fed the same batch of diet 2. Surprisingly, the tests showed that the animals had different urinary metabolite profiles. Rats from group “A” were predominantly excreting methylhydroxyphenyl-propionic acid (m-HPPA) while 16

Enquiries into the origin of the animals revealed that the animals that excreted m-HPPA originated from a different floor within the breeding unit than those animals that excreted HA”. However, when animals from each floor were housed together, the excretion profiles became harmonised after only 7 days2. Removing the animals from the environment of their barriered breeding units allowed bacterial species present in their intestines to populate all animals. In fact, a previous study published in 1997 by a Japanese team3, had already demonstrated the “infectious nature” of intestinal bacteria. In conclusion, we can assume that

“harmonisation of the urinary profile (of organic metabolites) after contact between the two groups of animals supports [the view] that differences in intestinal microflora might be responsible for the distinct profiles” 2.

probably through a weak but selective antibiotic action 6. In fact, chamomile oil’s antibacterial properties towards Helicobacter pylori have been well documented, inhibiting bacterial growth “in extraordinarily low concentrations of 0.0075 %” 7.

This view is strengthened by what happened to the urinary metabolites when the rats were treated with either saline or antibiotics. The antibiotic regimen suppressed the bacterial growth and its consequences on the profiles2.

Urinary Metabolites Provide Fungal Markers

An article published in Nature Review of Microbiology in May 2005 suggested using “the metabolite signature that is found in host fluids such as urine” to improve “the understanding of dysbiosis and gut micro-organism related diseases processes” 4. The researcher JK Nicholson stated that “several papers have detailed the identification of dynamic changes in the urinary levels of microbiotal products” in germ-free rats (bred and kept in a micro-organism free environment) as well as in conventional rats after they have been treated with antibiotics4. The changes of urinary organic metabolite profiles of germ-free rats have been studied when the animals were acclimatised to standard, not sterile, laboratory conditions. The associated changes in the gut microfloral communities can easily be observed by following the corresponding urinary profiles over a three week-period, the time needed by the gut microflora to stabilise5.

Study on Healthy Volunteers and Chamomile Tea Similar tests were applied to humans in relation to their response to chamomile tea ingestion. A single cup of chamomile tea was given every day to a group of healthy volunteers for a 10 day period. When their urine was tested at the end of this period, the samples showed modifications in microbial metabolites. Chamomile tea was then withdrawn and their urine retested after a further 10 day period. It was found that the metabolic signature had not reverted to its pre-dose condition, thus indicating that the chamomile tea had a rather profound and not easily reversible effect on the gut flora6. This surprising result suggests that chamomile tea reselects microbial populations in the human gut

Hence it could be possible to spot several fungal metabolites, such as arabinose and arabinitol, in the urine of patients suspected to suffer from intestinal fungal overgrowth. D-arabinitol is a typical metabolite of Candida albicans8. Its identification in the urine provides a clue to both the existence of candidiasis and its severity, providing us with important qualitative and quantitative data1. We must emphasise that the urinary metabolite signature evaluates microorganisms in situ and therefore prevents the unsatisfactory flaws rising from false positive and, especially, false negative results linked to stool cultures. Indeed, the main problem with stool cultures lies in the huge differences between the laboratory and the intestinal environmental conditions. Yeasts do not feel comfortable once excreted in the stools and many die or do not remain healthy enough to grow into observable colonies in the laboratory Petri dishes. Besides, most gut bacterial species do not tolerate oxygen, many of them being strictly anaerobic. Indeed, the large majority of the intestinal microflora has either never been cultured or cannot be cultured in standard conditions9.

Urinary Metabolites Provide Putrefactive Bacterial Markers Multiple markers can be obtained from both the presence and the overgrowth of a typical putrefactive bacterial genus. For example, Clostridium metabolises the aromatic amino acids phenylalanine and tyrosine into phenolic compounds, and tryptophan into indolic compounds10-12. In 1979, Chalmers (a pioneer in genetic testing on urinary organic acids) had already measured 4-hydroxyphenyl-acetic acid in urine as a screening method for small-bowel diseases and bacterial overgrowth syndromes13. 17

“Phenol, para-cresol and hydroxylated phenolsubstituted fatty acids are known to be the main products of tyrosine fermentation in anaerobic bacteria, whereas phenyl-acetate and phenylpropionate are formed from phenylalanine. (…) Indole, indole-acetate, and indole-propionate are all products of tryptophan metabolism”11. It might even be possible, in the future, to identify the species of Clostridium according to their specific profiles of urinary organic metabolites9. Clostridia represent a putrefactive genus, thus all the above-mentioned urinary metabolites will reflect an overgrowth of putrefactive bacteria. Test profiles of urinary organic acids associated with putrefactive microbial overgrowth include benzoate, hippurate, phenyl-acetate, phenylpropionate, cresol, hydroxy-benzoate, hydroxyphenyl-acetate, hydroxy-phenyl-propionate, 3,4-dihydroxy-phenyl-propionate, and indican14.

Urinary Metabolites Provide Fermentative Bacterial Markers Human tissues can produce D-lactic acid in extremely small amounts (in fact only nanomolecular concentrations), whereas it represents a major metabolic product of several bacterial strains within the human gut14. Multiple strains secreting D-lactate belong to fermentative species, many of them within the genus Lactobacillus15. A study published in 1991 had already shown that tricarballylate is another metabolite produced by intestinal bacteria, as it quickly appears when a conventional intestinal microflora is implanted in germ-free rats16. Tricarballylate is produced by aerobic bacteria that repopulate rat intestines, and it is considered as a fermentative marker16. Interestingly, an excessive production of tricarballylate has been blamed for the cause of magnesium deficiency known as grass tetany in ruminants17. This phenomenon results from the molecular structure: it contains 3 carboxylic groups ionized at gut physiological pH that can bind magnesium very tightly, triggering the magnesium malabsorption14.

An Everyday Diagnosis On a practical level, sophisticated databases 18

and experienced chromatography teams are much needed as more than 250 urinary organic metabolites “are either typically present or may be encountered in [human] urine”18. Fortunately for the patients, “a random specimen, preferably the first morning voiding when applicable, is an acceptable alternative” to the 24 hours urine collection18. Given that fluctuations on the ranges of excretion “mainly depend on individual metabolic variations rather than on dietary factors”19, no special diet is needed prior to the collection of the first morning urine sample. However, with a complete change of diet, significant metabolite variations will ultimately occur, but the shift will take some time.

Conclusion Intestinal microbial growth is accompanied by the release of products coming from their metabolism that tend to be absorbed by the intestinal lining and thereafter excreted in urine14. As a consequence, “detection of abnormally elevated levels of these products is a useful diagnostic tool for patients with gastrointestinal and toxicological symptoms” 14. Dysbiotic patients can benefit from an easy-tocollect urine test that facilitates the identification of fungal and/or bacterial overgrowths. In addition, the increase of specific markers can show-up overgrowths of either putrefactive or fermentative bacterial strains. Moreover, these urinary organic metabolite profiles bring insight not only into the existence but also into the severity of imbalances in the intestinal microflora, as they provide quantitative measurements. Such quantitative measurements represent another crucial advantage comparatively to stool cultures, as you would not assume that laboratory Petri dishes ensure growths proportional to what effectively occurs in human intestines, if the microbes grow at all... Perhaps the best proof that this diagnostic method gains popularity and may provide clues for treatment is a very recent article published in May 2010 about using urinary metabolic phenotyping to differentiate autistic children from their unaffected siblings and controls20. Differences in urinary metabolites (including hippurate) are observed between autistic and control children20,

whereas autism has been associated with intestinal dysbiosis and with Clostridium overgrowth21.

References: 1. Larsson, L., Determination of microbial chemical markers by gas chromatography-mass spectrometry--potential for diagnosis and studies on metabolism in situ. Review article. Apmis, 1994. 102(3): p. 161-9. 2. Williams, R.E., et al., Effect of intestinal microflora on the urinary metabolic profile of rats: a (1)H-nuclear magnetic resonance spectroscopy study. Xenobiotica, 2002. 32(9): p. 783-94. 3. Kitamura, S., et al., The role of mammalian intestinal bacteria in the reductive metabolism of zonisamide. J Pharm Pharmacol, 1997. 49(3): p. 253-6. 4. Nicholson, J.K., E. Holmes, and I.D. Wilson, Gut microorganisms, mammalian metabolism and personalized health care. Nat Rev Microbiol, 2005. 3(5): p. 431-8. 5. Nicholls, A.W., R.J. Mortishire-Smith, and J.K. Nicholson, NMR spectroscopic-based metabonomic studies of urinary metabolite variation in acclimatizing germ-free rats. Chem Res Toxicol, 2003. 16(11): p. 1395-404. 6. Wang, Y., et al., A metabonomic strategy for the detection of the metabolic effects of chamomile (Matricaria recutita L.) ingestion. J Agric Food Chem, 2005. 53(2): p. 191-6. 7. Weseler, A., et al., A novel colorimetric broth microdilution method to determine the minimum inhibitory concentration (MIC) of antibiotics and essential oils against Helicobacter pylori. Pharmazie, 2005. 60(7): p. 498-502.

Measurement of 4-hydroxyphenylacetic aciduria as a screening test for small-bowel disease. Clin Chem, 1979. 25(10): p. 1791-4. 14. Lord, R. S., and J. A. Bralley, Clinical applications of urinary organic acids. Part 2. Dysbiosis markers. Altern Med Rev, 2008. 13(4):292-306. 15. Bongaerts, G. P., et al., Role of bacteria in the pathogenesis of short bowel syndrome-associated D-lactic acidemia. Microb Pathog,1997. 22(5):285-93. 16. McDevitt, J., and P. Goldman, Effect of the intestinal flora on the urinary organic acid profile of rats ingesting a chemically simplified diet. Food Chem Toxicol, 1991. 29(2):107-13. 17. Schwartz, R., M. Topley, and J. B. Russell, Effect of tricarballylic acid, a nonmetabolizable rumen fermentation product of trans-aconitic acid, on Mg, Ca and Zn utilization of rats. J Nutr, 1988. 118(2):183-8. 18. Kumps, A., P. Duez, and Y. Mardens, Metabolic, nutritional, iatrogenic, and artifactual sources of urinary organic acids: a comprehensive table. Clin Chem, 2002. 48(5): p. 708-17. 19. Chalmers, R.A., et al., Urinary organic acids in man. II. Effects of individual variation and diet on the urinary excretion of acidic metabolites. Clin Chem, 1976. 22(8): p. 1288-91. 20. Yap, I. K., et al., Urinary metabolic phenotyping differentiates children with autism from their unaffected siblings and age-matched controls. J Proteome Res, 2010. 9(6):2996-3004. 21. Parracho, H. M., et al., Differences between the gut microflora of children with autistic spectrum disorders and that of healthy children. J Med Microbiol, 2005. 54(Pt 10):987-91.

8. Sigmundsdottir, G., et al., Urine D-arabinitol/L-arabinitol ratio in diagnosis of invasive candidiasis in newborn infants. J Clin Microbiol, 2000. 38(8): p. 3039-42. 9. Tannock, G.W., Analysis of the intestinal microflora using molecular methods. Eur J Clin Nutr, 2002. 56 Suppl 4: p. S44-9. 10. Elsden, S.R., M.G. Hilton, and J.M. Waller, The end products of the metabolism of aromatic amino acids by Clostridia. Arch Microbiol, 1976. 107(3): p. 283-8. 11. Smith, E.A. and G.T. Macfarlane, Formation of Phenolic and Indolic Compounds by Anaerobic Bacteria in the Human Large Intestine. Microb Ecol, 1997. 33(3): p. 180-8. 12. Smith, E.A. and G.T. Macfarlane, Enumeration of human colonic bacteria producing phenolic and indolic compounds: effects of pH, carbohydrate availability and retention time on dissimilatory aromatic amino acid metabolism. J Appl Bacteriol, 1996. 81(3): p. 288-302. 13. Chalmers, R.A., H.B. Valman, and M.M. Liberman,


Carbs’ Surprising Heart Disease Connection By Suzanne Dixon, MPH, MS, RD Fat, fiber, and protein all lower the glycemic index of meals and snacks. For years, conventional wisdom has held that avoiding the saturated fat found in red meat and high-fat dairy is one of the best dietary ways help prevent heart disease. But if new research is any indication, avoiding certain carbohydrates may be even better.

suggests that if simple carbohydrates replace saturated fat calories, this may increase heartdisease risk, not lessen it. Simply put: simple carbohydrates increase heart disease risk more than saturated fat.

Curbing carbs If you want to keep your ticker healthy, it makes sense to watch the saturated fat in your diet. However, be sure you don’t replace those fats with simple carbs. Some tips on how to do this: •

Watch the white foods. Try to limit the amount of refined grains you eat. These are found in white bread, pretzels, cakes, cookies, pies, and other processed foods.

The devil is in the details

Researchers followed 53,644 men and women with no history of heart disease to look at the connection between saturated fat, carbohydrates, and heart disease. Participants were between 50 and 64 years old at the start of the study and provided detailed information about their dietary and health habits.

Decode labels. Read ingredient lists. If you see the word “enriched” in the ingredient list, this is a tip-off that the food contains high GI, refined grains.

Pass on potatoes. White potatoes have a high GI. Instead try sweet potatoes, which have a lower GI and provide loads of heart-healthy nutrients, such as magnesium and potassium.

• The researchers looked at how substituting simple and complex carbohydrates into the diet in place of saturated fat affected heart attack risk. Glycemic index (or GI, a measure of how different carbohydrates, such as those found in potatoes and oatmeal, affect blood sugar levels) was used to classify carbohydrates as simple or complex. The higher the GI number, the higher the food will raise blood sugar in people who eat it.

Revealing results After following the participants for 12 years, the study authors found that for every 5% increase in simple carbohydrate calories that were substituted for saturated fat calories, there was a 33% increased risk of having a heart attack. Eating more complex carbohydrates did not increase heart attack risk.

Plain English, please For years, health experts have advised people to cut as much saturated fat out of their diet as possible to reduce heart disease risk. This study 20

Factor in fat, fiber, and protein. Fat, fiber, and protein all lower the GI of meals and snacks. Eating high GI foods along with healthy fat, such as nuts or nut butter; fiber; or protein will lower the overall GI of the meal. To put this in action, try an apple with peanut butter, instead of apple juice and pretzels, for example (Am J Clin Nutr 2010; 91:1764–8; Am J Clin Nutr 2010; 91:1541–2)

Suzanne Dixon, MPH, MS, RD, an author, speaker, and internationally recognized expert in chronic disease prevention, epidemiology, and nutrition, has taught medical, nursing, public health, and alternative medicine coursework. She has delivered over 150 invited lectures to health professionals and consumers and is the creator of a nutrition website acclaimed by the New York Times and Time magazine. Suzanne received her training in epidemiology and nutrition at the University of Michigan, School of Public Health at Ann Arbor.



The Multivitamin

The Multivitamin: the informed choice for preventative medicine

tested nutrients showed a statistically significant decline which the authors put down to “tradeoffs between yield and nutrient content”. Even organically-grown, pesticide-free produce cannot provide us with nutrients it does not contain!

The official line from health and nutrition specialists is that it is far better, and entirely possible, to obtain all of our essential nutrients from our diet alone. Of course this should be the case, and in an ideal world our nutrient-rich, whole-food diet would provide us with everything we need for optimum health and longevity. But, back in the real world, the Big 5 chronic diseases (namely, heart disease, cancer, diabetes, obesity and osteoarthritis) now constitute, according to the WHO, the biggest burden on health services worldwide and our immune systems appear to be losing the war.

Given that there is no immediate possibility of our soils regaining their former mineral content, supplementation has simply become a nutritional necessity in today’s world. Dr Jonathan Wright, MD, one of the world’s foremost experts in Nutritional Medicine, is very succinct on the subject. He presents us with two strategies for optimum nutrition:

Those of us who are able and informed are making every effort to maintain a healthy diet and lifestyle. Unfortunately, in spite of our efforts, years of nutrient-depletion in the soils intensively used for agriculture, as well as certain farming techniques and fertilisers used, means that we are still not receiving as many nutrients as we should. Statistics published from the 1992 United Nations “Earth Summit” set the average percentage of mineral depletion in soils at 85% for North America and at 72% for Europe (based on changes in soil composition from data gathered in 1936)i. A 2004 studyii took 43 common garden crops and compared nutrient data gathered in 1950 and again in 1999 for 13 nutrients. 6 out of the 13 22

1. Make sure that before we are born, we select parents, grandparents, and great-grandparents that have eaten a totally organically-grown whole-food diet, with 100% free-range animal protein and wild fish for their entire lifetimes. We must then continue to eat in the same fashion for our entire lifetimes. Explanation: Studies have shown that feeding mother animals nutrient-deficient diets can cause immune system and other malfunctions which remain detectable for the next three generations despite totally nutrient replete (but not supplemented) diets for those subsequent generations. Even if you or I eat “perfectly”, if our mothers, grandmothers, or great-grandmothers were nutrient-deficient, we can still have health problems responsive to supplementation that trace back one or more generations

2. Travel back in time to centuries during which all human food was by Nature organic, free range, and wild, a time when food was and had been available in sufficient quantity and variety to sustain healthy human life. Explanation: It is well-known that soils used for agriculture for years, worldwide, are depleted in many trace minerals. It is also known that the “NPK” fertilizers [Nitrogen, Phosphorous and Potassium] do not contain all the elements needed for optimal plant health. It is also well known that herbicides, pesticides, and other agricultural chemicals are detrimental to optimal health. Many foods are processed and refined, with key nutrients removed, and/or with sugars, salt, “trans” fats, and other detrimental-to-health items added. Recently, “genetically modified” (GMO) foods have been added to the “food” supply, which have already been observed to cause illness and death in experimental animals. He goes on to conclude, “As Strategies #1 and #2 (above) are (at present) impossible, it is indeed necessary to use a supplemental vitamin/mineral combination for the best chance of optimal health and metabolic functioning.” The benefits of multivitamin supplementation go far deeper than simply compensating for dietary deficits. They could literally be lifepreserving. Dr Honglei Chen, Head of the Aging and Neuroepidemiology Group at the U.S National Institute of Environmental Health Sciences has established that multivitamin use is associated with longer leukocyte telomeres among women. Telomeres, the end points on chromosomes, shorten with every cell division. When the telomere is gone, the cell can no longer divide which means that the longer the telomere, the longer-lived the cell. In essence, multivitamin use may slow the aging process.

Tellingly, micronutrient intake from foods was generally not related to telomere length, except for vitamins C and E. The benefits of regular, long term multivitamin usage over recent or sporadic usage appear in many studies. In 2009, a studyiv demonstrated that the long-term (over ten years) use of multivitamins and vitamin E were associated with a 16 and 28 per cent decreased risk of death from cardiovascular disease. And in his 2003 study on the use of multivitamins and colorectal cancerv, Eric J Jacobs concluded that long term usage, not recent, of a multivitamin did have a positive effect on colorectal cancer risk. Multivitamins do more than support our physical well-being. A randomized, double-blind and placebo-controlled studyvi of 215 healthy men aged between 30 and 55 showed that a multivitamin and mineral supplement was able to improve mood and mental performance, as well as reduce stress and fatigue. Its lead researcher, Pr David Kennedy commented “The assumption was made here that the men tested enjoyed typical nutritional status. However, the very fact of being able to improve mood, ratings of mental health and vigour and aspects of task performance by simple supplementation with B vitamins, Vitamin C and minerals indicates that the cohort must have been suffering from less than optimal micronutrient status at the outset.” Other recent studies demonstrating the benefits of multivitamin supplementation include a Chinese study demonstrating a positive effect of multivitamin usage on the body weight and LDL of obese Chinese women (February 2010, Wang et al) and a 2006 study showing that periconceptional use of multivitamins reduces the risk of preeclampsia (Lisa M Bodnar et al).

There are also those studies which raise questions on multivitamin usage. One such studyvii, begun iii The study consisted of data analysed from 586 in 1997 in Sweden, consisted of 35,329 cancerearly participants of the Sister Study, an ongoing free women completing a self-administered cohort prospective study of the healthy sisters questionnaire on their multivitamin use. Ten years of breast cancer patients. Dr Chen found that on, the follow-up research found a link between multivitamin users of the once-a-day variety multivitamin use and breast cancer risk. In 2007, had on average 5.1% longer telomeres, which the US National Institutes of Health published their corresponds to around 9.8 years less age-related findings from the AARP Diet and Health studyviii telomere loss. It was long-term multivitamin usage which found a link between excess multivitamin (greater than 5 years) which showed these benefits. usage and advanced prostate cancer.


However, experts are quick to point out these studies’ limitations and flaws and even the studies’ authors have concluded that the findings require more research. Experts reviewing the latter study point out that the extra risk was seen only in men with a family history of prostate cancer. Chronic diseases like cancer have long development times and are often triggered by events in earlier life, however, no data exists for either study on major contributory factors including genetic predisposition, childhood lifestyle and nutrient intake, current diet or quality of multivitamin used: were subjects eating a whole-food, unrefined diet? Were their multivitamins high potency, naturallysourced supplements or low-dose, over the counter ones, possibly synthetic? It is also important to note that many respected studies exist which directly contradict the data outlined above. In 1999 the Nurses’ Health Study reported that multivitamin use was associated with a significant decrease in breast cancer riskix. A study conducted by researchers from the Harvard Medical School, published in 2008, found no association at all between multivitamins and breast cancer risk, but did suggest that multivitamin use might reduce the risk of breast cancer for women consuming alcohol, and may also decrease the risk of sex hormone receptor negative breast cancers. In both of these, the presence of folic acid and B Vitamins in the multivitamin was credited with neutralising the harmful effects of alcohol and exerting a protective effect.x So, whilst it would appear that the experts are divided on the multivitamin-cancer risk issue, the one point on which they do unanimously agree is that the subject requires more research before definitive conclusions can be drawn. In fact, in response to public concern generated by the Swedish study, The American Institute for Cancer Research immediately counselled against stopping our daily multivitamin and pointed out that the relationship between supplements and cancer risk is far from clear. And there is the crux of the matter. In spite of the uncertainty, the majority of experts still believe that multivitamin supplementation, at least until more is known, should continue as before. Could it be that they too are convinced that a healthy diet and healthy behaviours may not be achieving what they once did, before soil depletion, pollution and 24

food-refining took their toll? It would certainly seem so. In June 2002, after a review of some 400 research studies, the Journal of the American Medical Association reversed its long standing stance against supplements stating “Most people do not consume an optimal amount of all vitamins by diet alone… appears prudent for all adults to take vitamin supplements.”xi

Endnotes: i. “Why do I need to supplement my diet with Colloidal Minerals”

ii. Journal of the American College of Nutrition, Vol. 23, No. 6, 669-682 (2004). Changes in USDA Food Composition Data for 43 Garden Crops, 1950 to 1999 (Donald R. Davis, PhD, FACN, et al) iii. AJCN. First published ahead of print March 11, 2009 as doi: 10.3945/ajcn.2008.26986. Multivitamin use and Telomere Length in Women. (Dr Honglei Chen et al) iv. Am J Epidemiol. 2009 Aug 15;170(4):472-83. Epub 2009 Jul 13. Use of supplements of multivitamins, vitamin C, and vitamin E in relation to mortality. (Pocobelli G, et al) v. Am J Epidemiol 2003; 158:621-628. Multivitamin Use and Colorectal Cancer Incidence in a US Cohort: Does Timing Matter? (Eric J Jacobs et al) vi. ScienceDaily 20 May 2010. 14 July 2010. Northumbria University. “Multivitamins Can Add Sparkle for Healthy Young People.” (Pr David Kennedy et al). vii. Am J Clin Nutr. 2010 May;91(5):1268-72. Epub 2010 Mar 24. Multivitamin use and breast cancer incidence in a prospective cohort of Swedish women (Susanna C Larsson, et al). viii. JNCI Journal of the National Cancer Institute 2007 99(10):754-764; doi:10.1093/jnci/djk177 Multivitamin Use and Risk of Prostate Cancer in the National Institutes of Health–AARP Diet and Health Study. (Karla A. Lawson, et al) ix. JAMA. 1999;281:1632-1637; Prospective Study of Folate Intake and the Risk of Breast Cancer (Shumin Zhang, MD et al) x. American Journal of Epidemiology 2008 167(10):11971206; doi:10.1093; A Prospective Study of Multivitamin Supplement Use and Risk of Breast Cancer (Ken Ishitani et al) xi. JAMA. Vitamins for Chronic Disease Prevention in Adults. 2002;287:3127-3129



Lutein Slows Vision Loss By Jane Hart, MD Lutein is important for healthy vision and is found in dark-green leafy vegetables such as lettuce, kale, and spinach. A diet rich in dark-green leafy vegetables is essential for eye health, and specific nutrients such as lutein that are found in these foods may have particular benefits for people who suffer from eye disorders. A new study in the Archives of Ophthalmology suggests that supplementing with lutein may slow vision loss in people who suffer from an eye disease known as retinitis pigmentosa.

the word “enriched” in the ingredient list, this is a tip-off that the food contains high GI, refined grains. The study authors point out that a daily dietary recommendation for lutein has not been established and that most Americans eat 1 to 2 mg per day. Prior studies, however, have shown that 6 mg per day of lutein supplementation is associated with a reduced risk of cataracts and age-related macular degeneration. The long-term safety of taking lutein supplementation has yet to be established. There are also a number of risks of taking high-dose vitamin A, so it is important to check with your doctor before taking dietary supplements in order to learn more about the risks and benefits.

Lutein plus vitamin A protects peripheral Tips for eye health vision • Eat a balanced diet. Along with other nutrients,

lutein is important for healthy vision and is found in dark-green leafy vegetables such as lettuce, kale, and spinach. This new study is another good reason to strive for those five servings of fruits and vegetables every day.

Retinitis pigmentosa refers to a group of hereditary diseases that affect the retina of the eye. The condition often starts in adolescence and slowly progresses through adulthood leading to partial vision loss or sometimes blindness. In this study, 225 non-smoking people aged 18 to 60 who had retinitis pigmentosa were randomly assigned to receive 12 mg of lutein or a control tablet (providing no treatment), and all participants received daily vitamin A (as 15,000 IU of retinyl palmitate). During the first year of the study participants were also advised to eat two 3-ounce servings of oily fish per week after a study showed benefit of DHA (docosahexaenoic acid) supplementation for retinitis pigmentosa.

Avoid unhealthy lifestyle behaviors. Smoking and drinking alcohol in excess may damage eye health, and both habits are also associated with lower serum lutein levels according to the study authors.

Wear sunglasses. Ultraviolet light from the sun can be damaging to healthy eyes but especially for people who suffer from eye disorders. Wear protective glasses and provide glasses for your children while enjoying the sunny outdoors.

Researchers followed the people in the study for Jane Hart, MD, board-certified in internal four years, collecting information from annual eye medicine, serves in a variety of professional roles exams and monitoring of blood serum lutein levels. including consultant, journalist, and educator. Dr. Results showed: Hart, a Clinical Instructor at Case Medical School in Cleveland, Ohio, writes extensively about health and • People who took lutein had a slower decline of wellness and a variety of other topics for nationally side (midperipheral) vision loss compared with recognized organizations, websites, and print the control group. Vision loss was significantly publications. Sought out for her expertise in the slower among those with the highest serum areas of integrative and preventive medicine, she lutein levels compared with those who had the is frequently quoted by national and local media. lowest. Dr. Hart is a professional lecturer for healthcare professionals, consumers, and youth and is a regular • Decode labels. Read ingredient lists. If you see corporate speaker. 26

Upcoming Events The internationally leading practice-oriented Hormone Therapy Seminars November 15-20, 2011

Hertoghe Medical School, 9 Avenue van Bever, 1180 Brussels, Belgium For more information see:

1st Latin-American Congress of the World Society of Anti-Aging Medicine (WOSAAM) October 7-9, 2011

S達o Paulo, Brazil For more information see:

Leading international practice-oriented Anti-aging Medicine Seminars (Proceedings in English)

November 15-20, 2011

Hertoghe Medical School, 9 Avenue van Bever, 1180 Brussels, Belgium For more information see:

Pro-aging Europe 2012 Seminar Congress March 4, 2012

Brussels, Belgium Warsaw, Poland For more information see:

All events supported by The World Society of Anti-aging Medicine (WOSAAM)

Italian Secrets

The secrets of Italians centenarians By Ascanio Polimeni, Regenera Research Group Are there centenarian secrets to a healthier and longer life? Recent Italian centenarian studies suggest that the application of a new endocrine approach, the science of syncrinology and hormonal harmony, may improve health and lengthen our life. Aging and related diseases are promoted by interactions between various factors: genetic factors, life style, environmental factors and others. Among these other factors, the progressive decrease with age of the production of sex hormones, growth hormone (GH), melatonin, thyroid hormones, DHEA, and in particular the loss of balance between anabolic (GH, DHEA, testosterone) and catabolic hormones (cortisol) and the loss of harmony among various hormonal systems seem to exert an important role in the promotion of the aging process. A review of the most important Italian studies about the connection between hormonal levels and balance and longevity demonstrates this. In three different studies published in the last years the department of Biogerontology of the University of Pavia checked the excretion rate of sulfatoxymelatonin (aMT6s), the major metabolite of melatonin, in healthy young and old people and centenarians. The total excretion rate of aMT6 clearly declined with age in all subjects, not only in healthy long living subjects. 28

But the circadian periodicity of melatonin secretion was maintained in centenarians, but not in the aged controls, who experienced a loss of the melatonin circadian rhythm. Since melatonin plays an important role as endogenous synchronizer of several biological hormonal (such as those of cortisol, GH, leptin, ghrelin) and non hormonal rhythms (blood pressure, body temperature and cytokines) and acts as a powerful free radical scavenger, the persistence of the circadian organization of melatonin secretion could be of great interest in successful aging and promoting longevity. In another study published in the Journal of Experimental Gerontology in 2008, the levels of anabolic hormones (IGF-1, DHEA and testosterone) were checked in a group of older men. The researchers showed that in older man a parallel age-associated decline in bioavailable testosterone, IGF-1, and DHEA sulfate secretion is associated with a higher mortality independent of potential confounders. They concluded the study saying that the ageassociated decline in anabolic hormone levels is a strong independent predictor of mortality in older men and that having multiple hormonal deficiencies rather than a deficiency in a single anabolic hormone is a robust biomarker of a declined health state in older persons. Similar conclusions were shown in a study done by the University of Parma where the neuroendocrine deregulation was investigated, and specifically the ratio between anabolic hormones - such as DHEA and testosterone - and catabolic steroids – such as cortisol.

The scientists tried to find connections between frailty and hormonal imbalance. Odd’s ratio for a highly significant increase in risk of frailty was demonstrated only when the three hormones were simultaneously considered (Odd’s ratio = 10.0 with 95% CI=1.6-6.4); the significance disappeared when each steroid was considered individually. The authors concluded that sarcopenia, the core of elderly frailty, can be seen as the direct consequence of the disruption of steroid hormone syncrinology. Consequently, the use of replacement treatment in order to delay the beginning of such steroid derangement might be a suitable strategy to improve the quality of life of man, whose life length has been significantly extended. But what’s the take home message of these studies’? We can say that the harmonious maintenance of biological rhythms (hormonal and not) and hormonal syncrinology through proper diet, stress control, adequate physical and sexual activity, and the administration of physiological doses of bio-identical hormones, are important strategies to improve longevity and successful aging. News flash from the in Chianti study:

How cognitive decline may be connected to DHEAS levels in the aged. Session: From Soil to Medical Practice (Italian Experience) By Professor Giorgio Valenti, ReGenera Reasearch Group

Background & aim of the study

Dehydroepiandrosterone (DHEA) and its sulfate ester (DHEAS) is the most abundant steroid circulating hormones in humans. DHEA and DHEAS levels decline with age in both sexes; this fall occurs concurrently with the onset of many of the common functional impairments typically encountered in older persons. It is quite documented that these steroids are produced also inside the brain, under the control of regulatory mechanisms different form those involved in adrenal secretion. Consequently the age related decline of cognitive performances was hypothetically connected with such modified steroid pattern. A number of studies in animals demonstrated that the administration od these steroids was able to enhance memory in several different models of young and aged animals and using various learning paradigms. In humans several observational and intervention studies have been realized. In the Massachusetts Male Aging Study DHEAS level was not a significant independent correlate of cognition. In the Endogenous Androgen Levels in Women across the Adult Life Span Study, DHEAS levels were strong significant correlates of performance in certain cognitive measures. Furthermore DHEA levels were not predictors of differential cognition decline in three large prospective cohort studies: the Rancho Bernardo Study (males and females), the Study of the Osteoporotic Fractures (females) and the Baltimore Longitudinal Study of Aging (males). However a trend towards an inverse association between DHEAS and rate of cognitive decline was found in two prospective cohort studies involving both males and females, namely a French communitybase cohort study and a study performed in a small sample of healthy older subjects of the populationbase Rotterdam Study. So far only six randomized controlled intervention clinical trials have been carried out to evaluate the possible effect of DHEA treatment on cognitive performances. In these studies the only significant improvement was on 29

Material & methods In light of the conflicting results between animal and humans studies and because little of the human data come from a populationrepresentative cohort including both men and women, we investigated whether DHEAS levels and cognitive function measured by the Mini Mental State Examination (MMSE) are related either cross-sectionally and/or longitudinally (three years) in the inChianti Study. 1034 residents aged >65 yr of the inChianti Study with data available on DHEAS and MMSE were randomly selected. MMSE was administrated at baseline and three years later. Among these 841 completed a 3-yr follow up. Independent factors associated with MMSE and DHEAS were carefully identified with the aim of a proper adjustment of data with potential confounders. A significant age-related decline of both DHEAS levels (p<0.001) and MMSE (p<0.001) was found. At enrolment DHEAS was significantly and positively associated with MMSE score, independently of

the attention performance following stress in one of the trials. age and other potential confounders (p<0.005). While stronger in males this finding is supported in both sexes. Finally low baseline DHEAS levels were predictive of larger decline of MMSE and such relationship was significant after adjusting for covariates (p<0.03).

Conclusions Our findings suggest that low DHEAS levels might represent a significant risk factor predisposing to age-related cognitive decline and that it is worthwhile verifying the clinical efficacy of hormone replacement treatment as a therapeutic tool. In face of the mostly negative clinical trials at the present time performed in healthy elderly subjects, it is remarkable that DHEA treatment recently was shown to promote a significant, albeit transient, effect on cognitive performance in a cohort of patients with well-defined Alzheimer’s diseases. It is desirable that new clinical intervention trials can be set up in the next future involving larger populations and protracted for a longer period.

Genetics, Stem cells & Progressive Lifespan medicine Tuesday November 15

Wednesday November 16

Thursday November 17

Prenatal, childhood, Brain hormone Genetic typing juvenile & geriatric therapies tests & Stem cells endocrinology Genetic Typing Prenatal & Pediatric Tests Endocrinology Brain Hormone • Basics • Prenatal influences that • Cardiovascular disaffect the endocrine Therapies

Pregnenolone deficiency and therapy Growth hormone treatment in adults

• Basics • GH’s beneficial

• • • • • •

eases Breast cancer Prostate cancer Alzheimer ‘s; neurodeg. diseases Osteoporosis Obesity Longevity

• •

glands and may increase the risk of age-related diseases Prenatal embryogenesis of the endocrine glands Hypothyroidism: prenatally, in childhood and adolescence and its treatment Cortisol deficiency and safe treatment in children Childhood aldosterone deficiency & excess Melatonin deficiency in children Vasopressin deficiency and enuresis Growth hormone deficiency & treatment in childhood Female hormone problems in adolescent girls, including genital underdevelopment Androgen deficiency in childhood and adolescence in males, including genital underdevelopment Puberty disorders: Delayed and precocious puberty Diabetes in children Oxytocin deficiency in children Autism: Hormone deficiencies and treatment Attention deficit disorder, hyperkinetism, difficult child Growth disorders Obesity in children

effects on agerelated diseases: The scientific eviGenetic typing and • dence hormone therapy: • Growth hormone • • Endocrine-related deficiency: signs polymorphisms and symptoms, lab • tests • How genetic typing tests may help to set • Laboratory tests: • up safer hormone IGF-1 levels within therapies the reference range • Nutrigenomics: associated with disease Diet, nutrient and lifestyle changes • Growth hormone • treatment • Associating IGF-1 Stem Cell Therapy and growth hor• What are stem cells mone therapy • • History of stem cell • Growth hormone therapy secretagogues • Growth hormone: • Diff. adult stem - em- • risks, benefits, bryonic cells controversies • Stem cell therapy • Tips on how to solve Application of stem • problems with GH cell therapy to dis• • Nutrients and food ease: influences on GH • Somatostatin • Heart regeneration Opioids after myocardial • infarction • New teeth formation • • Blindness reversal • • Neurodegenerative diseasesOsteoporosis Hands on training Geriatric session: Learn to • Diabetes Endocrinology practice hormone • Skin diseases therapy • Cornea repair Hormone therapy adapta• Down syndrome, etc. tions to elderly patients


Practical Workshops in

Anti-Aging Medicine Specialization Seminars Leading international practice-oriented Anti-aging Medicine Seminars

Brussels, Belgium November 15-20, 2011 Contact E-mail: Website: Phone: +32-(0)2-379.34.42 Mobile: +32-(0)479.25.61.43 Fax: +32-(0)2-732.57.43 Address: WOSAAM 9 Avenue van Bever, 1180 Brussels – Belgium

Anti-aging & Hormone Therapies I__I__I__I__I__I__I__I__I__I__I__I__I

Friday November 18 The anti-aging clinic & consultation

Anti-AgingClinic: start Anti-aging consult

•Anamnesis : Appointment, medical history, complaints

•Dietary advice •Digestion improvement •Correction of nutritional deficiencies •Physical examination •Laboratory tests

•Hormone tests •Nutritional tests

• • •

Functional – paramedical tests, cancer screening Interpreting/presenting test results to patients, Hormone therapies:

Patient cases: nutritional therapies

Genetic tests: for genital cancers: how to work with


 

Relaxin therapy : restore skin elasticity, hair volume, energy, blood glucose, no pain, Epithalon, thymalin: lifeextending and diseasereversing how to get, doses, safety Other exception peptides HCG: anti-pain, massive obesity: new frontiersy?

Exciting patients cases Hormone therapies and hormone conversion blockers : exciting practical info  Gut by acid-base balance  Vitamin, trace element, fatty acid & mineral therapies:  Amino acid therapies: Patients cases  Gut flora, digestive enzymes therapies 

Sunday November 20

Physical exam for hormone therapy Recognizing physical hormone signs and symptoms, of deficiency &

overtreatment of

• Growth hormone & IGF-1

• MSH • Oxytocin

● Vasopressin Melatonin Thyroid ● Calcitonin Parathormone Cortisol/glucocorticoid Pregnenolone ● DHEA

• • • • • • Aldosteronefludrocortisone • Insulin • Estrogen • Progesterone in women • Testosterone in women • Progesterone in men • Multiple hormone deficiencies in famous people

CAATS software :

hormone data on patient’s

Hands on training session: Learn to practice hormone therapy

Home DVD learning The major hormone therapies: REVIEW

• •

• • • • World Society of Anti-aging Medicine



• •

The official fellowship of the

BEST new & essential treatments to reverse aging in 2011

•Correction of hormonal

• Get your diploma in Anti-aging medicine

Saturday November 19 Nutritional & hormone therapy workshop

• • • • •

Thyroid treatment of mild & severe hypothyroidism with T4-T3, T4 & T3 Estrogen and progesterone therapy of pre-and postmenopausal women Testosterone treatment of men & women with testosterone deficiency DHEA therapy of DHEA deficiency Safe uses of cortisol therapy in cortisol-deficient patients Aldosterone deficiency: treatment Pregnenolone treatment Melatonin treatment Growth hormone treatment of GH deficiency Vasopressin/desmopressin therapy Oxytocin treatment MSH/melanotan treatment IGF-1 treatment Progesterone therapy in men

Home DVD learning Menstrual cycling Female hormone therapy Intensive hands on training Menstrual cycling with female hormone therapy

 Menstrual cycling in postmenopausal women with or without breast cancer

 Bio-identical female hormones for birth-control

Estradiol deficiency in men Intensive hands on training

• •

On stage life consultations Hands on training part 1 & 2

Hormone mesotherapy

• •

to reduce presbyopia and myopia Mesotherapy to reduce wrinkles

Nutritional therapy

• • •

Efficient micronutrient therapy for erectile dysfunction Silicone therapy Digestive tract improvement


Two exceptional new books or editions by

Dr. Thierry Hertoghe at

The Atlas of Endocrinology & Hormone Therapy 250 €, 327pages + DVD practical teaching Shows the physical signs and complaints of the 36 major hormone deficiencies and excesses that physicians encounter in their practice and can relieve. The book is unique. Next to about 500 exceptional pictures of patients with smaller physical endocrine signs, more than 200 additional pictures and figures, often not shown in the traditional atlas of endocrinology, the Atlas of Endocrinology & Hormone Therapy provides extensive schematic overviews of the many physical signs to make it all the more comprehensible enriched by a far reaching literature review of the signs and symptoms of hormone dysfunction, making it evidence-based. The Atlas is the ideal complementary help book to the Hormone Handbook and enables physicians to recognize the signs of hormone deficiencies and excesses to diagnose hormone dysfunction and to optimize the treatment. The abundant scientific references on the hormone signs and deficiencies help the physician to further deepen his knowledge to justify his hormone diagnoses and treatment.

Hormone Handbook, 2nd edition 290 €, 848 pages The practical hormone therapy book for physicians, this international bestseller covers the 18 most important hormone therapies. The second half of the book contains the abundant lists of scientific references for the application of each hormone therapy on mind, body, diseases and lifespan, including references on the major controversies. • Finding the best ways and products to treat hormone deficiencies • Solving problems that may occur during hormone treatment the best lists of references to justify the use of these • Therapies and get the lead in scientific controversies and debate • Medical board justification of the use of each of the hormone therapies MORE: + 30% practical information & updated references NEW: 6 major hormones NEW: Crucial data on cancer-protective hormones & lab tests Useful for physicians

The age of antibiotics may be coming to an endwhat can we turn to? By Paul Clayton, Ph.D.

Scientists speculate that the age of antibiotics may be coming to an end. This is because there has been a relentless increase in antibiotic resistance across all classes of drug. Furthermore, recent articles on antibiotic resistance in China paint an alarming picture of a near-future where antibiotics will have little therapeutic value (Heddini et al 2009). Sadly, the use of antibiotics inevitably leads to the selection of resistance traits; the overuse and misuse of antibiotics in medical and other situations makes it increasingly unlikely that we will be able to stay ahead in the war against infection. Important work in such areas as quorumsensing blockade may produce important new drugs, but these will not be available soon. Various alternatives have been proposed from the natural world, and this article reviews one of the most prominent candidates that being the lactoperoxidase system, specifically thiocynate ions as contained in associations of lactoperoxidase with thiocyanates (such as 1st Line®).

Lactoperoxidase/ Thiocyanates The enzyme lactopreoxidase (LPO) is one of the body’s major first-line defences against infection (Pruit ’87, Ratner & Prince 2000, Gerson 2000, Wijkstrom-Frei et al ‘03). LPO produces ions such as HOSCN, which have a broad spectrum of activity against gram-positive and gram-negative bacteria, HIV-1 and other viruses, moulds, yeasts, mycoplasma and protozoa (Pruitt & Reiter ’85, de Wit & van Hooijdonk ’96, Wang et al 2000, van Hooijdonk et al 2000, Seifu et al ’05, Fweja et al ’08). 32

LPO is critical for the control of pathogens in milk from lactating animals (Reiter et al ’86) including humans (Shin et al 2000). It also plays a key role in defending the respiratory and gastro-intestinal tracts (Wijkstrom-Frei et al ‘03). LPO utilises dietary thiocyanate as one substrate, producing hypothiocyanite (HOSCN) ions. These ions kill pathogenic bacteria (Table 1) via three separate mechanisms. They inhibit bacterial glycolysis; they inhibit bacterial nicotinamide adenine dinucleotide (NADH)/nicotinamide adenine dinucleotide phosphate (NADPH)– dependent reactions (Reiter & Perraudin ‘91); and they oxidise bacterial sulphydril groups (Slungaard & Mahoney ’91, Thomas & Aune ‘78). LPO also utilises iodine, forming hypohalide ions. These have an additional spectrum of anti-bacterial activity. Table 1: LPO activity in vitro: (number of strains tested) Bacteria • Escherichia coli (10) • Yersinia enterocolitica (4) • Klebsiella pneumoniae (13) • Klebsiella oxytoca (10) • Streptococcus agalactiae • Streptococcus mutans • Staphylococcus aureus • Salmonella species (12) • Shigella sonnei (15) • Listeria monocytogenes • Acinetobacter species (40) • Neisseria species (20) • Haemophilus influenzae(20) • Campylobacter jejuni (14) • Aeromonas hydrophila (8)

• Pseudomonas aeruginosa (6) • Capnocytophaga ochracea • Selenomonas sputigena • Wolinella recta • Enterobacter cloacae (12)

Viruses • Herpes simplex virus • Immunodeficiency virus • Respiratory syncytial virus

Yeasts • Candida albicans

Uniquely, HOSCN ions also have potent anti-viral activity. Many viruses have sulfhydryl groups on their coat (ie Mangold & Streeck ‘93); when these are oxidised (ie by thiocyanate) the viral coat structure is damaged or destroyed (Almeida et al ‘79).

certain specific circumstances (ie Leyer & Johnson ’93), the evolutionary historical evidence indicates that this is clinically insignificant. Moreover, most mammals utilize LPO / HOSCN on a daily basis and it remains an effective element in the innate immune system.

HOSCN ions are not toxic to human cells at the levels produced by LPO, and have little if any effect on probiotic species, making them a near-perfect antibiotic system. Furthermore, it is very difficult for microorganisms to acquire resistance to LPO; if it was easy for pathogens to become LPO-resistant, a key element in our immune system would have been disabled and we would not have survived as a species. Today, however, the LPO system is frequently compromised. Lactoperoxidase is a ferroprotein, and iron depletion / deficiency is one of the most common forms of dysnutrition. There are also growing problems with two of LPO’s substrates, thiocyanate and iodine. Thiocyanates are derived from dietary glucosinolates (in brassica), or from cyanogenic glycosides (in beans, sweet potato and millet). Since 1950, UK consumption of fresh vegetables has fallen by 24% (Hinton ‘08). Iodine depletion is becoming more prevalent, due inter alia to reductions in salt intake and the use of (non-iodinated) sea salt (Li et al ‘06, Nawoor et al ‘06). The net effect of depletion in iron, iodine and cyanogens on LPO activity is likely to be very significant in reducing our ability to ward off infections.

With regard to safety, it should be pointed out that the level of hypothiocyanous ions in associations of lactoperoxidase with thiocyanates are genera lly well within safe levels and well below the limit of any excess in levels of thiocyanate ions produced within the body (Borgers & Junge ’79, Medizinische ’82, WHO ‘95).

Due to its chemistry, LPO is not a suitable therapeutic tool; if the milk-derived enzyme were to be consumed it would, like other milk proteins, be digested and rapidly rendered ineffective. However, the bactericidal effects of LPO can be mimicked and amplified by delivering HOSCN ions directly. This technology was initially developed in France for food plant sterilisation, and subsequently to sterilise salad leaves. It is used as an antiseptic in Belgium, and has been adapted by the WHO for bulk milk sterilisation in China and Korea (FAO/WHO ‘05). We have reviewed the possibility that the extensive use of HOSCN might encourage the development of microbial resistance strategies, and believe that this is unlikely. Only a small number of intrinsically LPO-resistant microorganisms are known (ie Oram & Reiter ’66). While resistance may be acquired in

The association of lactoperoxidase with thiocyanates The association of lactoperoxidase with thiocyanates has been on the market as a patented formula that makes up into a drink containing hypothiocyanite and hypothiocyannous ions, identical to those in tears, saliva and milk. These ions are a critical defence against a wide range of pathogens including bacteria, yeasts, fungi and viruses; many of which they destroy on contact. Until recently, the unstable hypothiocyanite ions could not be stored. In a technical breakthrough, an association of lactoperoxidase with thiocyanates has been shown to enable the ions to be produced immediately prior to use so they can be consumed ‘fresh’, whenever required. For the first time, hypothiocyanite ions can be used as a supplement. These bio-identical immune molecules differ from antibiotics in two ways: 1. The ions are very small molecules, with a molecular weight of around 90. They therefore diffuse further and faster though tissues than the much larger synthetic antibiotics. 2. They kill a surprisingly wide range of diseasecausing micro-organisms, but unlike synthetic antibiotics do not damage probiotic species such as lactobacilli and bifidobacteria. Our immune systems and these beneficial bacterial species have co-evolved, and have ‘learned’ to co-exist. 33

This association of lactoperoxidase with thiocyanates has been shown to be more efficient when early used, at the first symptom of an infection for example. Often only one intake the first day is required. If symptoms persist another kit can be consumed the following day. Persons with more serious symptoms may need to use the association of lactoperoxidase with thiocyanates up to twice a week, dependent upon need. For those who want to prevent the symptoms of infection the association of lactoperoxidase with thiocyanates seems useful when used once every few months. And let us rememeber that hypothiocyanite ions are not toxic to human cells, they appear to have excellent tissue penetration and have little if any effect on probiotic species, making them a near perfect antibiotic system.

Summary In the war against infectious micro-organisms, where we are currently losing ground, associating the intake of lactoperoxidase with thiocyanates seems useful and supported by scientific data. For the first time, it enables the clinician or indeed any user to utilise one of the most powerful elements in our array of immune defences, namely the innate immune enzyme lactoperoxidase (LPO). In the body, LPO utilises dietary thiocyanates from such sources as brassica vegetables to produce HOSCN ions, which kill a wide range of bacterial and viral pathogens (see Table 1, below). Uniquely, and as would be expected from an innate immune defence, this wide spectrum of anti-microbial activity does not include the essential probiotic species which are immune to LPO activity.

normally use to produce HOSCN ions outside the body. These ions are then ingested, mimicing the endogenous effects of the enzyme exactly. Given the known efficacy and safety of the LPO / HOSCN system, and access to preliminary clinical trial data, I regard the development of this system as a medical break-through. I believe that the development of the LPO / HOSCN system is as important as the discovery of penicillin, and will make as great an impact on infection control. To the bureaucratic mind, however, it presents a substantial problem. First direct devolves infection control to the end-user, who now has direct access to a safe, food-derived anti-infection strategy. This is the internal equivalent to anti-septics, which everyone can use, and thus runs counter to the interests of the pharmaceutical industry, their profit margins and regulatory bodies. There is no question about the value of the enzyme system. The only question is how long this anomaly will be allowed to continue before big Pharma and its regulatory muscle either forcibly re-classify First Line as a drug, or suppress it altogether.

References 1. Almeida JD, Bradburne AF, Wreghitt TG. The effect of sodium thiocyanate on virus structure. J Med Virology 1979. 4(4):269-277 2. Babineau TJ, Hackford A, Kenler A, Bistrian B, Forse RA, Fairchild PG, Heard S, Keroack M, Caushaj P, Benotti P. A phase II multicenter, double-blind, randomized, placebo-controlled study of three dosages of an immunomodulator (PGG-glucan) in high-risk surgical patients. Arch Surg. 1994 Nov;129(11):1204-10. 3. Babineau TJ, Marcello P, Swails W, Kenler A, Bistrian B, Forse RA. Randomized phase I/II trial of a macrophagespecific immunomodulator (PGG-glucan) in high-risk surgical patients. Ann Surg. 1994 Nov;220(5):601-9.

Lactoperoxidase therefore has all the attributes of an ideal antibiotic, and this has lead many scientists to explore its therapeutic uses. All 4. Borgers D., Junge B., Thiocyanate as an indicator of previous attempts, however, have failed because tobacco smoking. the commercial enzyme is a dietary protein derived from milk. When eaten, LPO is rapidly broken 5. Preventive Medecine 8: 351-357 (1979) down in the stomach and small intestine and its enzymatic activity is lost. 6. Brousseau M, Miller SC. Enhancement of natural killer An association of lactoperoxidase with thiocyanates may constitute a far more intelligent approach. It uses phase-bound lactoperoxidase remotely, supplying it with the substrates it would 34

cells and increased survival of aging mice fed daily Echinacea root extract from youth. Biogerontology. 2005;6(3):157-63.

7. Czop JK, Austen KF â&#x20AC;&#x2DC;85: A b-glucan inhibitable receptor on human monocytes: its identity with the phagocytic


receptor for particulate activators of the alternative complement pathway. J Immunol 1985; 134: 2588-2593. 8. de Felippe J J, da Rocha-Silva F M, Maciel FM, Soares A de M, Mendes NF: Infection prevention in patients with severe multiple trauma with the immunomodulator beta 1-3 polyglucose (glucan). Surgery, Gynecology and Obstetrics 1993; 177(4): 383-388. 9. Dellinger EP, Babineau TJ, Bleicher P, Kaiser AB, Seibert GB, Postier RG, Vogel SB, Norman J, Kaufman D, Galandiuk S, Condon RE. Effect of PGG-glucan on the rate of serious postoperative infection or death observed after high-risk gastrointestinal operations. Betafectin Gastrointestinal Study Group. Arch Surg. 1999 Sep;134(9):977-83. 10. Di Luzio NR, Williams DL: The role of glucan in the prevention and modification of microparasitic diseases. In: Assessments of chemical regulation of immunity in veterinary medicine. Gainer JH, ed. NY: Scientific, Medical and Scholarly Pub., 1983 11. FAO/WHO Technical Report 2005. Benefits and Potential Risks of the Lactoperoxidase System of Raw Milk Preservation. Report of a FAO/WHO technical meeting, Rome, Nov-Dec ‘05 12. FDA ’99. Over-the-counter drug products containing colloidal silver ingredients or silver salts. Department of Health and Human Services (HHS), Public Health Service (PHS), Food and Drug Administration (FDA). Final rule. Fed Regist 64 (158): 44653–8. August 1999

to swine influenza virus by increased production of interferon-gamma and nitric oxide. J Vet Med B Infect Dis Vet Public Health. 2004 Mar;51(2):72-6. 20. Kernodle DS, Gates H, Kaiser AB: Prophylactic AntiInfective Activity of Poly-(1-6)-beta-D—Glucapyranosyl(1-3)-beta-D-Glucapyranose Glucan in a Guinea Pig Model of Staphylococcal Wound Infection. Antimicrob Agents & Chemother 42:545-549, ‘98 21. Kiermeier F, Kuhlman H, Thiocyanate forms and doseage. Münch. Med. Wochenschr. (1972) 22. Leyer GJ, Johnson EA. Acid adaptation induces cross-protection against environmental stresses in Salmonella typhimurium. Appl Environ Microbiol. 1993 Jun;59(6):1842-7. 23. Li M, Eastman CJ, Waite KV, Ma G, Zacharin MR, Topliss DJ, Harding PE, Walsh JP, Ward LC, Mortimer RH, Mackenzie EJ, Byth K, Doyle Z. Are Australian children iodine deficient? Results of the Australian National Iodine Nutrition Study. Med J Aust. 2006 Feb 20;184(4):165-9 2. 24. Available from file 25. Mangold CM, Streeck RE. Mutational analysis of the cysteine residues in the hepatitis B virus small envelope protein. J Virol. 1993 Aug;67(8):4588-97 26. Medizinische und biologische Bedeutung der thiocyanate (Rhodanide) Veb Verlag Volk (1982) – Ed. W.Weuffen (Berlin)

13. Fisher H, 2009. Mechanism and Function of DUOX in the Epithelia of the Lung. Antioxidants and Redox Signalling 11(10):1-14

27. Nawoor Z, Burns R, Smith DF, Sheehan S, O’Herlihy C, Smyth PP. Iodine intake in pregnancy in Ireland--a cause for concern? Ir J Med Sci. 2006 Apr-Jun;175(2):21-4.

14. Fweja LW, Lewis MJ, Grandison AS. Challenge testing the lactoperoxidase system against a range of bacteria using different activation agents. J Dairy Sci. 2008 Jul;91(7):2566-74.

28. NCCAM ’06. Colloidal Silver Products. National Center for Complementary and Alternative Medicine. December 2006.

15. Gerson CJ, Sabater M, Scuri A, Torbati R, Coffey JW, Abraham I, Lauredo R, Forteza A, Wanner M, Salathe WM, Abraham WM, Conner GE. 2000. The lactoperoxidase system functions in bacterial clearance of airways. Am. J.Respir. Cell Mol. Biol. 22:665–671. 16. Harger-Domitrovich SG, Domitrovich JW, Ruby BC. Effects of an Immunomodulating Supplement on Upper Respiratory Tract Infection Symptoms in Wildland Firefighters Medicine & Science in Sports & Exercise. 40(5):S353. 17. Heddini A, Cars O, Qiang S, Tomson G. Antibiotic resistance in China--a major future challenge. Lancet. 2009 Jan 3;373(9657):30.

29. Oram JD, Reiter B. The inhibition of streptococci by lactoperoxidase, thiocyanate and hydrogen peroxide. The oxidation of thiocyanate and the nature of the inhibitory compound. Biochem J. 1966 Aug;100(2):382-8. 30. Pruitt KM, Reiter B. 1985. Biochemistry of peroxidase system: antimicrobial effects. In The Lactoperoxidase System: Chemistry and Biological Significance. K. M. Pruitt and J. O. Tenovuo, editors. Marcel Dekker, Inc. New York. 143–178. 31. Pruitt, K. M. 1987. The salivary peroxidase system: thermodynamic, kinetic and antibacterial properties. J. Oral Pathol. 16:417–420.

18. Hinton WL. Supply & Demand for Vegetables in the UK. ISHS Acta Horticulturae 72

32. Rada B, Leto TL. Oxidative Innate Immune Defenses by Nox/Duox Family NADPH Oxidases. Egesten A, Schmidt A, Herwald H (eds): Trends in Innate Immunity. Contrib Microbiol. Basel, Karger, 2008, vol 15, pp 164–187

19. Jung K, Ha Y, Ha SK, Han DU, Kim DW, Moon WK, Chae C: Antiviral effect of Saccharomyces cerevisiae beta-glucan

33. Rasmussen, LT, Konopski Z, Oian P, Seljelid R; Killing of Escherichia coli by mononuclear phagocytes


and neutrophils stimulated in vitro with beta-1, 3-D-polyglucose derivatives, Microbiol Immunol 36(11):1173-1188. 1992. 34. Rasmussen, LT and Seljelid, R.: Novel Immunomodulators With Pronounced In Vitro Effects Caused by Stimulation of Cytokine Release, J Cell Biochem; 46:60-68. 1991. Quote: “Beta-1, 3-D-polyglucose derivatives protect mice against otherwise lethal bacterial infections.” 35. Rasmussen LT, Seljelid R, Dynamics of blood components and peritoneal fluid during treatment of murine E. coli sepsis with beta-1, 3-D-polyglucose derivatives. I: Cells. Scand J Immunol 32(4): 321-331. Oct 1990. 36. Rasmussen LT, Seljelid R, Dynamics of blood components and peritoneal fluid during treatment of murine E. coli sepsis with beta-1, 3-D-polyglucose derivatives. II. Interleukin 1, tumor necrosis factor, prostaglandin E2 and leukotriene B4, Scand J Immunol 32(4): 333-340. Oct 1990. 37. Rasmussen LT, Seljelid R: The modulatory effect of lipoproteins on the release of interleukin 1 by human peritoneal macrophages stimulated with beta 1 -3D-polyglucose derivatives. Scand J Immunol 1989; 29: 477-484. 38. Rasmussen LT, Seljelid R, Production of prostaglandin E2 and interleukin 1 by mouse peritoneal macrophages stimulated with beta-1, 3-D-glucan derivatized plastic beads Scand J Immunol 26(6): 731-736. Dec 1987. 39. Rasmussen, LT, Fandrem. Jr., and Seljelid R., Dynamics of Blood Components and Peritoneal Fluid During Treatment of Murine E. Coli Sepsis with beta-1, 3-D-polyglucose Derivatives; Scand. J Immunol 63:73-80 1985. 40. Ratner AJ, Prince A. Lactoperoxidase. New recognition of an “old” enzyme in airway defenses. Am J Respir Cell Mol Biol. 2000 Jun;22(6):642-4. Review. 41. Registry of Toxic Effects of Chemical Substances ’77, German drug use 42. Reiter, B., V. M. Marshall, L. Bjorck, and C. G. Rosen. 1976. Nonspecific 43. bactericidal activity of the lactoperoxidases-thiocyanate– hydrogen peroxide 44. system of milk against Escherichia coli and some gramnegative pathogens. 45. Infect. Immunol. 13:800–807. 46. Reiter B, Perraudin J-P. 1991. Lactoperoxidase: biological functions. In Peroxidases in Chemistry and Biology, Vol. I. J. Everse, K. E. Everse and M. B. Grisham, editors. CRC Press. Boca Raton, FL. 144–180. 47. Seifu E, Buys EM, Donkin EF. 2003. Significance of the lactoperoxidase system in the dairy industry and its

potential applications: a review. Trends in Food Science and Technology, 16:137-154 48. Shin, K., M. Tomita, and B. Lonnerdal. 2000. Identification of lactoperoxidase in mature human milk. J. Nutr. Biochem 11:94–102. 49. Slungaard A, Mahoney JR Jr. Thiocyanate is the major substrate for eosinophil peroxidase in physiologic fluids. Implications for cytotoxicity. J Biol Chem. 1991 Mar 15;266(8):4903-10 50. Talbott S, Talbott J. Beta 1,3/1,6 glucan decreases upper respiratory tract infection symptoms and improves psychological well-being in moderate to highly-stressed subjects. Agro Food Industry Hi-Tech. January/February 2010. Vol 21, n1 51. Talbott S, Talbott J. Effect of Beta 1,3/1,6 Glucan on Upper Respiratory Tract Infection Symptoms and Mood State in Marathon Athletes. Journal of Sports Science and Medicine (2009) 8, 509-515 52. TGA ’05. Regulation of colloidal silver and related products. Australian. Therapeutic Goods Administraion. 2005-11-09. 53. Thomas EL, Aune TM. Lactoperoxidase, peroxide, thiocyanate antimicrobial system: correlation of sulfhydryl oxidation with antimicrobial action. Infect Immun. 1978 May; 20(2): 456–463. 54. Van Hooikdonk ACM, Kussendrager KD, Steijns JM. 2000. In vivo antimicrobial and antiviral activity of components in bovine milk and colostrums involved in non-specific defence. Br J Nut, 84 (Suppl.1): S127-134 55. Wang H, Ye X, Ng TB. First demonstration of an inhibitory activity of milk proteins against human immunodeficiency virus-1 reverse transcriptase and the effect of succinylation. Life Sci. 2000 Oct 20;67(22):274552 56. Wijkstrom-Frei C, El-Chemaly S, Ali-Rachedi R, Gerson C, Cobas MA, Forteza R, Salathe M, Conner GE. Lactoperoxidase and human airway host defense. Am J Respir Cell Mol Biol. 2003 Aug;29(2):206-12. 57. De Wit JN, van Hooijdonk CCM. 1996. Structure, function and applications of lactoperoxidase in natural antimicrobial systems. Netherlands Milk and Dairy Journal, 50:227-244 58. Mansell PWA, Ichinose I-I, Reed RJ, Krements ET, McNamee RB, Di Luzio NR: Macrophage-mediated destruction of human malignant cells in vivo. J Nat Cancer Inst 1975; 54: 571-580. 59. Onderdonk AB, Cisneros RL, Hinkson P, Ostroff G: Antiinfective effect of poly-beta-1,6-glucotriosyl-beta 1,3glucapyranose glucan in vivo. Infection & Immunity 60:1642-1647, ‘92 60. Robertsen B, Engstad RE, Jorgensen JB. Beta- glucans as 37

Immunostimulants in fish. Immune Responses l994, V. 1 Fair Haven, NJ, USA. Song Y-L, Hsieh Y-T. Immunostimulation of tiger shrimp hemocytes for generation of microbicidal substances: analysis of reactive oxygen species. Developmental and Comparative immunology. Vol.l, No.3, pp.201-209, 1994. Elsevier Science. 61. Suzuki, Hashimoto K, Ohno K, Tanaka H, Yadomae T Immunomoddulatory by orally administered beta glucan in mice. Int J Immunopharmacology 1989;11:761-769 62. Tzianabos AO, Cisneros RL; Prophylaxis with the immunomodulator PGG glucan enhances antibiotic efficacy in rats infected with antibiotic-resistant bacteria, Ann NY Acad Sci 797: 285-287; Oct 1996. 63. Vetvicka V, Terayama K, Mandeville R, Brousseau P, Kournikakis B, Ostroff G: Pilot Study:Orally-Administered Yeast Beta1,3-glucan Prophylactically Protects Against Anthrax Infection and Cancer in Mice; J Am Nutraceutical Assocn 5:1-5, ‘02 64. Wakshull E, Brunke-Reese D, Lindermuth J, Fisette L, Nathans RS, Crowley JJ, Tufts JC, Zimmerman J, Mackin W, Adams DS. PGG-glucan, a soluble beta-(1,3)-glucan, enhances the oxidative burst response, microbicidal activity, and activates an NF-kappa B-like factor in human PMN: evidence for a glycosphingolipid beta-(1,3)-glucan

receptor. Immunopharmacology. 1999 Feb;41(2):89-107. 65. Washburn WK, Otsu I, Gottschalk R, Monaco AP: PGGglucan, a leukocyte-specific immunostimulant, does not potentiate GVHD or allograft rejection. J Surg Res 62, 179-83, ‘96 66. Williams D.L. and Diluzio N.R.; Modification of Experimental Viral Hepatitis by Glucan Induced Macrophage Activation. In the Reticuloendothelial System and Pathogenesis of Liver Disease, Liehr and Grun, eds. Elsevier/North Holland Biomedical Press; pp. 363-368. 1983. 67. Williams D.L. and Diluzio N.R.; Glucan-Induced Modification of murine Viral Hepatitis. Science (1980), 208: 67-69. 1980. 68. Williams D.L., et al; Protective Effect of Glucan in Experimentally Induced Candidiasis. J. Reticuloendothel; Soc 23: 479-490. 1978. 69. Williams D.L, Diluzio NR, Glucan induced modification of experimental Staphylococcus aureus infection in normal, leukemic and immunosuppressed mice. Adv Exp Med Biol 121(A): 291-306. 1979


from childhood to old age Tuesday November 15

Wednesday November 16

Brain hormone therapies

Male & female hormone problem-solving seminar Andrology: Hormone therapy solutions

Thursday November 17 Prenatal, childhood, juvenile & geriatric endocrinology Prenatal & Pediatric

Endocrinology for male problems • Prostate hypertrophy, prostatitis, prosta- • Prenatal influences on tism Reducing excessive estradiol & endocrine glands with high PSA levels Treating prostate cancer Pregnenolone risk of age-related diseases patients with androgens Infertility deficiency & • Hypothyroidism: prena• Short penis: increase the size of the therapy tally, in childhood and penis  Small testicles: increase the size Growth hormone of the testicles adolescence & therapyt treatment in adults • Peyronie’s disease Varicocèle • Cortisol deficiency and • Gynecomastia  Varicose veins •Basics safe treatment in children • Stronger beard growth • Childhood aldosterone •GH’s beneficial • Male pattern baldness deficiency & excess effects on age• Sports performance related diseases: • Melatonin deficiency in scientific evidence Hormone therapy solutions for sexual children performances •GH deficiency: signs Men: Erotic fantasies, pheromones, sex- • Vasopressin deficiency and enuresis & symptoms, lab ual arousal, sexual sensitivity, erectile tests dysfunction, coitus, ejaculation, orgas- • Growth hormone defimic intensity, premature ejaculation, ciency & treatment in •Lab tests: IGF-1 sperm childhood levels within the reference range • Women: Attracting a partner • Female hormone problinked with disease (pheromones), sexual arousal, erotic lems in adolescent girls, fantasies, sexual sensitivity, coitus underdeveloped genitals • GH treatment frequency, dyspareunia, orgasm  • Androgen deficits in boys • Associating IGF-1 infertility Cervix ripening & adolescents, incl. and GH therapy underdeveloped genitals Gynecology: Hormone therapy solutions • GH secretagogues for female problems • Puberty disorders: De• GH: risks, benefits, • Menstrual cycle disorders: short cycles, layed - precocious puberty • Diabetes in children controversies menorrhagia, dysmenorrhea, • Oxytocin deficiency •Tips on how to solve a/hypomenorrhea, , PMS, cyclical mi• Autism: Hormone deficiengraine, swelling problems with GH cies and treatment cysts  Small breasts • Attention deficit disorder, •Nutrients and food •• Breast Enlarged breasts Ovarian cysts, hyperkinetism, difficult child influences on GH • Endometriosis Fibroids • Growth disorders Somatostatin • Hirsutism; Urinary incontinence • Obesity in children Opioids • Birth control pill Hot flushes Geriatric Endocrinology • Treating breast cancer women with Hormone therapy adaptafemale hormones tions to elderly patients Brain Hormone Therapies

Hands on training session: Learn to practice hormone therapy

Home DVD learning

Aesthetical Endocrinology

Acne  Dry skin Thin skin Premature aging skin, elasticity loss Vitiligo & hyperpigmented spots Eczema, psoriasis, mycosis Petechiae, hematomas Poor wound healing  Keloids Hair loss: Alopecia totalis & diffusa, alopecia pelada  Hirsutism Male pattern hair lossGrey hair Vulvar lichen Varicose veins  Hormone therapies to improve the physical appearance Eyes: dry eyes, swollen eyelids, conjunctivitis, dark circles under the eyes, sunken eyes, excessive eyebrow protrusion


Home DVD learning

Aesthetical & Longevity Endocrinology

Aesthetical Endocrinology

Nose: swollen, too thin nose, too small nose Face: hypotrophy of the jaw bones, chin hypotrophy, sagging cheeks, too thin face Shoulders and arms: muscle wasting; Hands: how hormones influence the appearance of the hands Mouth: inflammed/retracted gums Lips: thin, swollen Chest: gynecomastia Abdomen: fat - droopy belly Thighs: cellulite, sagging inner sides of the thighs Body silhouette: sagging, scoliosis, kyphosis, lordosis, excessive thinness, overweight Legs: varicose veins, ankle ulcers Feet: flat feet, osteoarthritis deformation Longevity Endocrinology

Basic mechanisms Hormone therapies to live longer


Practical Hormone therapy workshops

Hormone Therapy Specialty

The internationally leading practice-oriented Hormone Therapy Seminars Brussels, Belgium November 15-20, 2011 Get your diploma in Hormone Therapy

Friday November 18

Saturday November 19

Sunday November 20

Practical Hormone Therapy Workshop

Nutritional & hormone therapy workshop

Physical exam for hormone therapy

Patient case studies presented by experienced physicians

BEST new & essential treatments to reverse aging in 2011

Patients with • allergies • muscle stiffness • low stress resistance, exhaustion • chronic fatigue, insomnia • memory loss • chronic fatigue • alopecia ... • male pattern hair loss, back pain, neuronal atrophy • excessive weight gain in a child • massive obesity in a child • depression. On stage consults with Dr T. Hertoghe ic tests: for genital cancers: how to work with



 

Relaxin therapy : restore skin elasticity, hair volume, energy, blood glucose, no pain, Epithalon, thymalin: lifeextending and diseasereversing, doses, safety Other exception peptides HCG: anti-pain, massive obesity: new frontiersy?

Exciting patients cases Hormone therapies and hormone conversion blockers : exciting info  Gut by acid-base balance  Vitamin, trace element, fatty ac. & mineral therapies:  Amino acid therapies: Patients cases • Gut flora, digestive enzymes therapies • Amino acid lab tests 

Recognizing physical hormone signs and symptoms, of deficiency & overtreatment of • Growth hormone & IGF-1 • MSH • Oxytocin ● Vasopressin • Melatonin • Thyroid ● Calcitonin • Parathormone • Cortisol/glucocorticoid • Pregnenolone ● DHEA • Aldosteronefludrocortisone • Insulin • Estrogen • Progesterone in women • Testosterone in women • Progesterone in men • Multiple hormone deficiencies in famous people CAATS software : hormone data on patient’s

Hands on training session: Learn to practice hormone therapy

Home DVD learning The major hormone therapies: REVIEW

CONTACT: E-mail: Website: Phone: +32-(0)2-379.34.42 Mobile: +32-(0)479.25.61.43 Fax: +32-(0)2-732.57.43

Address: International Hormone Society 9 Avenue van Bever 1180 Brussels – Belgium

The official fellowship of the International Hormone Society

• Thyroid treatmentmild & severe hypothyroidism with T4-T3, T4 & T3

• Estrogen and progesterone therapy of

Home DVD learning

Menstrual cycling Female hormone therapy Intensive hands on training Menstrual cycling with female hormone therapy

Menstrual cycling in postmenop.

women with or not breast cancer

pre-and postmenopausal women

• Testosterone treatment of men & women Bio-identical hormones for birth• • • • • • • • • • •

with testosterone deficiency DHEA therapy of DHEA deficiency Safe uses of cortisol therapy in cortisoldeficient patients Aldosterone deficiency: treatment Pregnenolone treatment Melatonin treatment Growth hormone treatment of GH deficiency Vasopressin/desmopressin therapy Oxytocin treatment MSH/melanotan treatment IGF-1 treatment Progesterone therapy in men


Estradiol deficiency in men Intensive hands on training

• •

On stage life consultations Hands on training part 1 & 2

Hormone mesotherapy

• •

to reduce presbyopia and myopia Mesotherapy to reduce wrinkles

Nutritional therapy

• • •

Efficient micronutrient therapy for erectile dysfunction Silicone therapy Digestive tract improvement

Compounding Strategies By: Peter Cornelius, Pharmacist Receptura International Compounding Pharmacy 60438 Frankfurt / Main

Taking into Account the Pharmacokinetics of Bioidentical Hormones after Oral, Transdermal and Transbuccal Administration Hormones including bio-identical hormones must eventually pass through the liver. There they are filtered out of the blood stream and metabolised into forms that can be eliminated from the body via the bile or urine. Hormones taken orally (tablet or powder capsules) will be absorbed from the intestines and then pass through the liver immediately. Consequently a large portion of the hormone dose will be metabolised in the liver before it is carried to the body cells. For this reason higher doses of hormones are necessary if they are administered in oral forms (tablet or powder capsules form). Whereas this is no problem for most of the patients, in others this kind of application may cause side effects. The liver may render the hormones ineffective or it becomes overworked by breaking down the hormones. This may result in side effects such as fluid retention, weight gain, nausea, headaches, high blood pressure or even blood clots. In such cases the hormone therapy has to be stopped or the application form has to be changed to avoid the absorption from the intestine into the liver. Natural (bio-identical) hormones can be easily administered in forms that are directly absorbed

into the blood stream before they pass through the liver. These forms can be • Hormones encapsulated with oil • Hormone patches • Creams and gels • Lozenges (troches) Using these forms also enables smaller doses to be administered as the hormones can perform their function on the body cells before the liver breaks them down.

Bio-Identical Hormones encapsulated with oil, As hormones have lipophilic properties the encapsulation with oil has a significant effect on their bioavailabilty. Recent studies with natural progesterone have shown that the absorption and thus the bioavailability are significantly influenced not only by the vehicle but also by the particle size of the hormones (5-6). Suspending (dissolving) micronized progesterone in oil with longchain unsaturated fatty acids results in a stable compound which leads to significant serum levels within two hours. After a loading phase of five days a permanent progesterone concentration could be achieved for a period of more than 36 hours.


By micronization the surface of the hormone crystal is very much enlarged so that the hormones can be absorbed very quickly and most of them avoid to be metabolized. The data of ongoing studies for orally administered hormones show significantly the synergism of the combination of a high grade micronization and the suspension in oil. The dissolution of natural hormones in oil is very stable so that the hormones are protected from the stomach acid. The absorption takes place together with the exogenously absorbed lipids (triglycerides) in the form of chylomicrons (lipoproteins) directly into the lymphatic system and then into the blood stream. The greater the degree of unsaturation of the fatty acids in an oil the more rapid is the onset of chylomicron synthesis (1-4). Capsules are an application form with high flexibility concerning the dosage and combination of hormones to suit the individual patient.

Bio Identical Hormones in form of Patches and creams / gels are absorbed very well across the skin into the small blood vessels in the subcutaneous layer of the skin. The use of hormone creams and gels gives also more flexibility. They can be tailor made to meet the individual needs of the patient, and can be compounded to provide any variety of natural hormones such as the three different types of natural estrogen or the combined estrogens (estradiol, estrone and estriol = tri-est) or (estriol and estradiol = bi-est), natural progesterone, testosterone and DHEA. Also the doses can easily be adjusted in such creams and gels. The recommended amount of the cream - generally half a teaspoon or one pump - depending on the administration system â&#x20AC;&#x201C; has to be massaged deeply into the dry skin of the inner upper thigh twice daily.

placed under the tongue or between the upper gum and the cheek. There they should remain by dissolving slowly (ca 5 minutes). The hormones are absorbed by the small blood vessels under the surface of the mucous membrane of the cheek. It is important that the lozenges are not chewed, sucked or swallowed, as otherwise the hormones will end up in the intestines and pass straight through the liver. The doses used in the lozenges are generally higher than those used in the creams. Also the lozenges can be tailor made to suit the individual, using any possible combination, and amounts of natural hormones.

References 1. Whitehead MI, Townsend PT, Gill DK, Collins WP, Campbell S. Absorption and metabolism of oral progesterone. Br Med J 1980; 280: 825-7. 2. Maxson WS, Hargrove JT. Bioavailability of oral micronized progesterone. Fertil Steril 1985; 44: 622- 6. 3. Chakmajian ZH, Zachariah NY. Bioavailability of progesterone with different modes of administration. J Reprod Med 1987; 32: 443-8. 4. Padwick ML, Endacott J, Matson C, Whitehead MI. Absorption and metabolism of oral progesterone when administered twice daily. Fertil Steril 1986; 46: 402-7. 5. Pharmacokinetics of estradiol, progesterone, testosterone and dehydroepiandrosterone after transbuccal administration to postmenopausal women. Wren BG, Day RO, McLachlan AJ, Williams KM. Climacteric. 2003 Jun;6(2):104-111. 6. Pharmacokinetic characteristics, efficacy, and safety of buccal testosterone in hypogonadal males: a pilot study Dobs AS, Hoover DR, Chen MC, Allen R.Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

Bio Identical Hormones in form of Lozenges / Troches Another very good option is to administer the hormones via the transbuccal route by using lozenges / troches. Hormonal lozenges have to be 40

Join Sao Paulo with the three days of the

of the

1st Latin American Congress World Society of Anti-Aging Medicine V International Symposium of Hormonal Physiology

Anti-aging medicine starts in the embryo

Octobre 7-9, 2011





Anti-aging Hormone therapies

Official organizing societies

Latin American’s better congress in South America’s largest city

The best anti-aging treatments

Leading International Medical Authorities

Join the two days where WARSAW is the Capital of the World of science and anti-aging medicine ...

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Leading international medical authorities

Contact: E-mail: Website: Fax: +48 12 6324388

ADVANCED CLINICAL NUTRITION 2011 SPECIAL TOPIC: Immunity and Cancer Friday 02 and Saturday 03 September 2011

European Laboratory of Nutrients Regulierenring 9, 3981 LA Bunnik, The Netherlands Phone: 0031 (0)30 2871492; Fax: 0031 (0)30 2802688 E-mail: For latest information Contact person (participants): Ada van Lent Contact person (organization): drs. J. Breijer

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