Lucas Zarraga
Senior Thesis | 2025
Epidemiology of Non-Alcoholic Fatty Liver Disease: A Survey from a Community-based
Screening Program in South Texas
Lucas Zarraga
Abstract/Prospectus
Non-alcoholic fatty liver disease has been a major concern in the field of gastroenterology due to its presence in 20-30% of the general population. In addition to adults and elderly people, an increasing proportion of adolescents and children are also experiencing progressions of higher severity like nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). NAFLD is caused by the excess accumulation of fat in the liver, leading to conditions of metabolic syndrome, like high levels of blood pressure and triglycerides, affecting the disease’s presence and progression. NAFLD’s pathogenesis is also influenced by heredity and chronic diseases, leading to certain genetic disparities among various ethnic groups, particularly Mexican-Origin (MO) adults, experiencing NAFLD more often than others at increased stages of severity. Socioeconomic factors influencing annual income and access to healthcare and medicine are also considered when viewing our data.
This research reports the epidemiologic characteristics of NAFLD in a community-based research clinic in South Texas. The data was collected at the beginning of my summer immersion program, beginning during June 2024 and continued remotely until November 2024. This study aims to provide a simple, crosssectional study of the prevalence of NAFLD among residents of McAllen, Texas. This study also aims to support the accuracy of FibroScan as an NAFLD diagnostic method and to find treatments, whether medically or economically, that tend to the disadvantages that lower-income residents and Latinos face in having NAFLD.
Introduction
What is hepatic steatosis? Also known as non-alcoholic fatty liver disease (NAFLD), or metabolic dysfunction-associated steatotic liver disease (MASLD), it is the build-up of extra fat in one’s liver from various factors other than alcohol. Fat in the liver is normal until it composes about 5-10% or more of one’s liver weight, leading to steatosis. There is a high risk of steatosis for those who possess metabolic syndrome, which are a set of conditions such as obesity, high cholesterol, high fat and triglycerides, and high blood pressure and blood sugar levels (1).
In fact, a study conducted using the Clinical Practice Research
Datalink (CPRD) of the UK found that NAFLD and NASH patients displayed increased rates of obesity, type 2 diabetes mellitus (DM), and hypertension when doing comparative analysis with a control group (2).
However, there are many other contributors to steatosis and fibrosis that also give rise to NAFLD through different pathways, which also possess complexities involving other factors, such as diet and genetic predisposition. Insulin restriction (IR), oxidative stress, esterification of glycerol and free fatty acids (FFA), mitochondrial dysfunction, endoplasmic reticulum (ER) stress, bacterial overgrowth, glucocorticoids, and a number of inflammatory cytokines and adipokines are all factors that contribute to the presence of NAFLD and its progression to NASH, and later, end-stage cirrhosis. This can cause greater risks of possessing hepatocellular carcinoma (HCC), a common type of liver cancer, in patients (1).
In addition, pediatric NAFLD is prevalent in approximately 3-10% of all individuals from North and South America, Australia, Europe, and Asia; factors such as race, sex, ethnicity, and variability in metabolic factors all influence NAFLD prevalence in certain populations (3). Much knowledge surrounding the epidemiology of NAFLD is still yet to be discovered. Although many studies and laboratories measure aminotransferase (ALT)
levels in patients to help diagnose NAFLD, it is reported by most that 80% of NAFLD patients have regular ALT levels (3). This noticeable discrepancy between ALT levels and fatty liver signifies the importance of proper non-invasive diagnostic methods to properly identify NAFLD in patients, preventing the disease’s continuous progression to NASH and more severe stages of liver disease. Prevalence of NAFLD can also tend to greatly increase in adolescents due to more insulin resistance and sex hormones present during puberty, as well as a tendency to take up unhealthy diets (3).
Despite knowing all these factors, there is still much research needed to uncover other ways that the pathogenesis of NAFLD can be attributed to. In addition, when considering the multiple pathways to the pathogenesis of NAFLD, there are, though rare at this stage, a variety of complications for patients. Some include: weakness, fatigue, extreme tiredness, and discomfort in the abdomen due to ascites, or fluid build-up in the belly. Similarly, the progression to NASH/fibrosis will normally not have too many symptoms, other than tiredness and pain in the upper right area of one’s abdomen. However, once patients’ livers begin to have severe scarring, being closer to the stage of cirrhosis (which can occur after having NAFLD for many years), increasingly worse symptoms start appearing. These include: extreme itching, jaundice (yellowing of eyes and skin), spider veins, hepatic encephalopathy (behavior changes and confusion caused by liver health problems), a swollen belly from ascites, increased bleeding and bruising, and higher risk of HCC. Given the current rise of obesity around the globe, and that 37% obese people worldwide possess NAFLD (1), it is important to also recognize which types of ethnic groups have this disease spread in their populations.
Latino populations, especially those in the U.S., are disproportionately affected by fatty liver disease and all of its stages, especially when compared to non-Latino white and black
populations (4). Three general conditions that contribute to the widespread cases of NAFLD among Latinos are: prevalence of chronic diseases (such as diabetes and/or metabolic syndrome), genetic predisposition, and various socioeconomic factors that prevent access to healthcare systems. Firstly, it is important to recognize that metabolic syndrome’s impact towards the presence of NAFLD is influenced by ethnic factors (4). One study that supported Latinos’ increased prevalence of NAFLD over African Americans showed that Latinos tend to have higher intrahepatic triglyceride levels and visceral fat, both which are strongly correlated with NAFLD, while African Americans, despite having higher rates of obesity, generally are less prevalent with NAFLD due to lower amounts of visceral fat. Increased diabetes among Latino populations also plays a factor in NAFLD cases (4). Next, in terms of genetic factors, many genome-wide association studies (GWAS) have proved effective in identifying patterns of heritability involved in the presence of NAFLD, many of which are found in Latinos. One study shows that a common gene found in many Hispanics called PNPLA3-I148M plays a large factor in NAFLD development through increased fat accumulation in the liver (5). This was especially true for Latino children who have this gene as opposed to those in European and African American populations (3).
Finally, it’s important to acknowledge that a variety of socioeconomic factors play a role in Latinos’ high number of NAFLD cases. With more than 1 out of 4 Latino adults living at or below the poverty line, low-cost foods that are strongly linked to obesity are heavily relied upon. Studies of Latinos assimilating into the U.S. throughout generations also rationalizes high prevalence of NAFLD. The first generation would tend to have higher fruit/vegetable content, while those following would increase their fast food/soda intake and lower fruit/vegetable content (3). Other factors like language barriers, lack of healthcare coverage, mistrust in healthcare systems, and transportation can all explain Latinos’
increased development of NAFLD. It’s also important to recognize that lack of discipline, interest, and time were major factors that contributed to Latinos’ low-use of lifestyle therapy, which contains recommended methods such as exercise and/or dieting to help prevent or reverse NAFLD (3).
Keeping in mind the ever-increasing population of Latinos in the U.S., with a number of them being undocumented immigrants, it’s important to also learn how diagnosis can be improved so that the public can recognize the seriousness of NAFLD’s rapid spread throughout the world. Large numbers of undocumented Latino immigrants can also lead to inaccurate data regarding NAFLD’s impacts on those communities (3), posing a challenge on providing proper diagnostic approaches and medical treatments. There are many methods in determining NAFLD’s presence, including blood sample tests, ultrasonography, MRI scans, and liver biopsies. Liver biopsy is able to track liver inflammation grade, steatosis, and fibrosis when removing thin tissues of the liver from the patient. The diagnosis method utilizes the METAVIR and Scheur scoring system to properly measure liver inflammation and fibrosis scores, respectively. Liver inflammation in patients with chronic hepatitis B, a long-term liver infection that makes people prone to liver cancer, has 5 grades: G0, G1, G2, G3, and G4 (6). Fibrosis was graded into 4 categories, which are S0 = absence of fibrosis; S1 = portal fibrosis without septa, or areas of scarring tissue; portal fibrosis with rare septa, S3 = high amounts of septa without liver cirrhosis, and S4 = end-stage cirrhosis (6).
One widely used method of diagnosis of fatty liver disease is FibroScan. Also known as transient elastography, FibroScan is an economical and non-invasive method to assess liver steatosis and fibrosis by sending ultrasound-waves into the liver via liver stiffness measurement (LSM). A study conducted at the Liver Unit of Bir Hospital in Nepal was done to find out whether or not CAP scores from FibroScan positively correlated with USG of steatosis
and other covariates (7). Liver scans via FibroScan can only be reliable if there are 10 conducted with an appropriate probe that are generated with a success rate of 60% or greater (7). FibroScan was also able to detect that 26 patients in the study diagnosed with NAFLD via ultrasonography (USG) did not actually have it. This was due to the patients’ obesity, leading to subcutaneous and visceral fat blurring the imaging of USG, while FibroScan was able to properly assess liver steatosis and fibrosis that correlate directly with NAFLD (7).
In this study, we assessed the prevalence of NAFLD from a community-based screening program for NAFLD, being conducted by McAllen Research, LLC. We have analyzed the different CAP, kPa, and other valuable data from patients to further understand: NAFLD’s demographic prevalence in McAllen, a variety of methods needed to aid in diagnostic gaps and disparities among Latino populations, supporting the credibility of FibroScan as a fatty-liver diagnosis method, and next steps involving therapies and ways to aid in the prevention of NAFLD development and its further progressions. Although the NAFLD screening program is a 3-year, industry-funded research, this paper mainly focuses on the data gathered over the months of June to November of 2024, coinciding with my senior thesis project.
Methods
After completing the necessary patient-privacy and clinical research training, I was part of a one-month immersion program at McAllen Research, LLC. A total of 6 months’ worth of FibroScan readings from patients in McAllen, Texas on liver steatosis and fibrosis was collected for this study. To protect patient privacy, all data was de-identified per standard procedures governed by the Health Insurance Portability and Accountability Act (HIPAA). The source data was secured in a cloud-based clinical trial database, maintained at McAllen Research, LLC. This community-based
screening program is provided free of charge to volunteers and has been approved by a local institutional review board (IRB).
To be eligible to participate, the volunteers were either residing or working in McAllen, Texas. Volunteers must not consume alcohol more than 3 standard drinks per week, no prior viral hepatitis or other metabolic liver diseases.
Transient elastography, or FibroScan, was used in assessing the steatosis and fibrosis of all patients. The FibroScan procedure starts with the operator sitting down next to the patient’s right side, making sure one hand controls the FibroScan probe position (placed between armpit to hip bone) while the other holds the probe weight. During the 10 performed scans, it’s crucial to have the patient lie in a ‘banana-shape’ exposing the right rib cage area while positioning the probe to be at the center of the liver, otherwise it will read either the patient's lower lobe or their lungs, leading to an inaccurate reading.
Results and Discussion
Demographics of McAllen Residents in Study Pool
Baseline demographics (N=282) n (%) n(%)
Gender Males, 240 (85) Females, 42 (15)
Age, mean+/- SD per gender 58+/- 11 52+/- 15
Ethnicity Hispanic, 254 (90) Non, Hispanic, 28 (10)
Prior diagnosis of NAFLD Yes, 21(7.5) No, 261 (92.5)
BMI (> 30) Yes, 198 (70) No, 84 (30)
Prior diagnosis of Type 2 DM Yes, 169 (60) No, 113 (40)
Currently on Type 2 DM medications Yes, 85 (30) No, 197 (70)
Table 1. Demographic characteristics of volunteers who underwent screening for NAFLD in McAllen, Texas
As expected, the majority of the volunteers were males, with median age in the 50s, and reporting to be of Hispanic ethnicity. There are significant metabolic comorbidities including obesity and diabetes that are untreated. The vast majority of volunteers have not been diagnosed with NAFLD. This demonstrates a significant unmet need for awareness, education and preventative screening in this underserved population.
Figure 1. Average CAP scores throughout June to November with standard deviation. June: CAP - 274.975, Std Dev - 53.185. July: CAP - 278.97, Std Dev - 50.421. August: CAP - 269.86, Std Dev53.35. September: CAP - 279.1, Std Dev - 55.959. October: CAP289.948, Std Dev - 71.565. November: CAP - 261.08, Std Dev63.688.
Figure 2. Average kPa scores throughout June to November with standard deviation. June: kPa - 6.043, Std Dev - 4.578. July: kPa6.231, Std Dev - 3.504. August: kPa - 7.012, Std Dev - 4.525. September: kPa - 6.732, Std Dev - 4.783. October: kPa - 8.117, Std Dev - 5.877. November: kPa - 8.816, Std Dev - 6.684.
Figure 3. Negative correlation value (r=-0.252) between mean CAP and kPa scores throughout June to November.
Throughout the 6-month study, average CAP score remained beneath 300 but always above 260, staying relatively at the same level with July and October having patients with the highest CAP scores (Figure 1). Mean kPa started off lower in June, but gradually rose until November with the highest kPa average of 8.8. (Figure 2). The correlation of average CAP and kPa throughout the study is slightly negative at a value of -0.252 (Figure 3). Most of our patients (n=254; 90%; Table 1) were of Latino origin, meaning that data involving lack of type 2 DM and NAFLD diagnosis and medications are representative of the Latino communities in McAllen.
After examining our study pool of 282 patients across the months of June to September (Table 1), we noticed that the FibroScan readings and data regarding access to prior diagnosis and medicine have aligned with public data in regards to genetic and diagnostic disparities in Latinos with NAFLD. Despite this, a
lot less patients during the months of June to September qualified for the McAllen NAFLD study due to the qualifying threshold of kPa being greater than or equal to 7 and that all of the months, except August, had an average kPa score of less than 7. However, during October and November, lots more ended up qualifying for the study since average kPa was 8.117 and 8.816, respectively.
The slight negative correlation (r=-0.252) of CAP with kPa throughout the 6-month period of data shows how increase in CAP does not always have to correlate with kPa. There are other forms outside of metabolic syndrome and poor dietary lifestyle leading to liver steatosis that can contribute to liver fibrosis, as well as certain conditions that can lead to simple scarring in the liver without excessive fatty liver build-up. Chronic illness and genetic disparities in Latino communities come into play when considering how patients with higher fibrosis levels, but not with consistently high steatosis, were from Latino background. Despite this, a majority of our patients had a BMI of greater than or equal to 30 (n=198, 70%; Table 1), meaning that most of our study pool had obesity and some forms of metabolic syndrome caused by fatty build-up in the liver.
Supporting our findings of prevalent obesity and NAFLD in our patient group, a study done by Tesfai et. al showed that NAFLD prevalence in the study pool of MO adults was 41%; 2 of 5 Hispanic adults have NAFLD, and within those that do, 2 of 3 Hispanic individuals also have NASH (9). This also matches with the fact that most scanned patients did not qualify for the study since most of them measured to have a kPa of lower than 7, especially in the earlier part of the 6-month scanning period. While Tesfai’s overall proportion varies across different studies, it’s still clear how health-disparities in Latinos are getting worse with the increased relative risk of NAFLD and NASH compared to other study groups of different ethnicities (9).
One study by Gerardo Heiss examined 9,789 women and 6,530 men of Latino origin. Men who were Puerto Ricans,
Mexicans, Cubans, Dominicans, and people of Central and South American origin had the highest prevalence of cardiometabolic abnormalities. There was also a strong positive correlation in age when it came to having an increasing percentage of men and women who possessed cardiometabolic abnormalities (8). Our study also showed that the majority (n=240; 85%; Table 1) of our study pool were males, while the rest (n=42; 15%; Table 1) were female. Not only does this align with the majority of Latinos in our own study that possessed obesity according to their BMI, but it also goes to show the lack of previous diagnosis and medical attention that Latinos tended to receive. Most of our patients (n=261; 92.5%; Table 1) have never had a prior diagnosis of NAFLD before the community-based scanning program. Many of them (n=197; 70%; Table 1) are also not on any Type 2 DM medications. Even the most simple steps of making local health clinics easily accessible for adults of Mexican-origin can be a large step in providing necessary diagnosis and medical attention for NAFLD and its progressions.
Highlighting the importance of accessibility to diagnosis to prevent negative effects of NAFLD, Amernia et al. conducted a study with 205 patients with NAFLD with a mean age of 42.96 years with standard deviation of 10.97 years. They utilized fatty liver disease diagnosis methods and compared them with FibroScan to determine its credibility in diagnosis. Alternative diagnosis methods included Fibrosis-4 (FIB-4), aspartate aminotransferase (AST) to platelet ratio index (APRI), and aspartate aminotransferase/alanine aminotransferase (AST/ALT) ratio, which are simple serum based tests (10).
According to FibroScan reading results, 94 patients (45.9%) possessed F1, 67 patients (32.7%) had F2, 29 patients (14.1%) had F3, and 15 (7.3%) had F4 fibrosis. This study also revealed that FibroScan kPa scores have a strong correlation with APRI (0.667), a moderate correlation with FIB-4 (0.572), and a weak correlation with AST/ALT ratio (r=0.251) (10). This shows
how these alternative diagnosis methods largely agree with the way FibroScan diagnoses NAFLD in patients. However, considering the variety of the correlation coefficients, it also means that liver fibrosis is not the most important factor in determining NAFLD’s presence. Other potential factors that FIB-4, ALT/AST, and APRI could account for may be patient age, genetic factors, or exposure to other kinds of molecules and/or chemicals that are influenced by lifestyle. Alongside having the proper diagnostic methods for NAFLD, it’s important to have healthy lifestyle modifications like exercise and dieting that can be crucial in preventing NAFLD progression and symptoms.
On the other hand, FibroScan CAP scores had an even lower correlation with APRI (0.046), FIB-4 (0.057), and even a negative correlation with AST/ALT ratio (-0.048) (10). This continues to support the idea that metabolic syndrome, while known to be largely responsible for the rise of NAFLD, is not a sole set of factors for the reason 30% of the general population have it. In fact, the negative correlation with AST/ALT also strongly suggests that alternative diagnosis methods rely on detecting completely different factors outside of liver steatosis that contribute to NAFLD development.
Looking more into FibroScan’s diagnostic efficacy, a study conducted by Jiang et al assessed the FibroScan’s accuracy for liver inflammation in patients with chronic hepatitis B (CHB), who possess a high risk of death from cirrhosis and liver cancer. 1185 patients with CHB were participated in the study; 75% (n=894) were male, 25% (n=291) were female, and about 55% (n=658) patients were hepatitis B e antigen (HBeAg) positive with CHB, while 45% (n=527) were HBeAg negative with CHB (6). Median age in the proportion of negative HBeAg was 37 years, which was 6 years older than the positive HbeAg group (31 years)(P < 0.001) (6). The study indicates the strong significance in presence of HBeAg affecting NAFLD presence, while acknowledging how age’s influence on the disease when HBeAg is not present. This
makes it important in considering how patients of Latino background may possess HBeAg in greater amounts and how it may build off of other genetic and socio-environmental factors that influence NAFLD’s increased cases in MO adults. In addition, Jiang et al found that out of 273 patients with hepatic steatosis, there were more cases found in men (n=230, 84%) and less in women (n=43, 16%)(P<0.001). They also found that fatty liver disease was more prevalent in the HBeAg negative group (n=142, 27%) than in the HBeAg positive group (n=131, 20%)(P=0.004) (6). Jiang et al trialed FibroScan on patients when they had an empty stomach or 2 hours after food consumption in the morning, performed by 3 operators with training background by Echosens with a training certificate. FibroScan had an overall test success rate >90%, with fibrosis scores ranging from 2.4 - 72 kPa; mean kPa was 11.96. Liver biopsy found that out of the biopsy tissues from the 1185 patients, 18% (n=208) had fewer than 10 portal areas (PAs), while 82% (n=977) had more than 10 PAs. Fibrosis stage and liver inflammation grade were positively correlated with one another (the Spearman’s rho = 0.829, P < 0.001). FibroScan LSM also showed a positive correlation with the inflammation grade (r=0.450, p < 0.001). It definitely would have been helpful for us to utilize and access more measurements of liver fibrosis and inflammation levels in patients’ liver to get a better sense of how severe it was for most patients to have high BMI, no type 2 DM medications, and no prior diagnosis of NAFLD.
Various causes that contribute to the rise of NAFLD that are not necessarily linked to liver steatosis are cell death, sterile inflammation, disturbances in gut microbiota, and morphogens inducing fibrogenic and progenitor response (11). This also signifies the steps needed in creating and advancing a variety of therapies for patients who are bearing these kinds of conditions. One promising therapy that was tested in the study conducted by Machado MV et. al was Vitamin E; this was specifically effective for non-diabetic patients with NASH (11). On the other hand,
ursodeoxycholic acid was tested and proved to have a limited role in therapy against NAFLD (11).
At the same time, it’s important to recognize that several therapies still need further investigation for their efficacy, supporting exactly how it’s still uncertain as to how many therapeutic paths can be taken in aiding patients with NAFLD. Machado MV et. al also found that pentoxifylline and probiotics are emerging therapeutic approaches with promising preliminary results, but still need to undergo larger clinical trials to better understand their efficacy and safety profiles (11). Similar to how a large portion of patients in our study have Hispanic background, Machado MV et. al also showed the complex interplay between genetic predisposition and environmental factors contributing to heterogeneity of disease presentation (11). While there are many alternative therapies, the study also showed that exercise and dietary changes were cornerstone lifestyle modifications in fighting against NAFLD. This very well applies to our study pool given that steatosis and BMI levels were very high across the 6month study period.
Similar to our study, Garcia et. al conducted a study on associated risk factors in a community-based sample of Mexicanorigin adults in the Cameron County Hispanic Cohort in Texas; sample size of 307 patients. NAFLD prevalence was shown to be 50.5%; 60.7% of them had obesity, while 60% of them had diabetes, suggesting a strong association with metabolic syndrome. 65.2% of NAFLD patients were female and 34.8% were male. Most significant differences between individuals with and without NAFLD was BMI, weight, waist circumference, and liver fibrosis (12). The PNPLA3 gene also had a significantly positive correlation with liver steatosis (beta = 9.5; 95% CI, 2.5, 16.6; P = 0.008; r = 0.08) (12). Age was also shown to play a factor in the disease presence shown with a 4.7 dB/m increase in steatosis along with a 10-year increase in age.
Garcia et. al. also utilized the US Department of Agriculture Automated Multiple-Pass Method in order to properly assess three 24-hour dietary recalls for MO patients (12). In addition, the Nutrition Data System for Research was used in analyzing the nutrition data and the Healthy Eating Index (HEI) was used in assessing diet quality (12). These resources would have been helpful in terms of assessing factors of nutrition and overall health of patients in our 6-month study pool, further validating the significance of dietary observation in tracking NAFLD in patients. They would have also made a good addition in terms of what we had in patients records that provided a general profile of patient nutrition and lifestyle by giving insight into what kinds of common dietary regulations can be maintained in order to control NAFLD.
In terms of gathering more information to get a better sense of patient conditions, Alexander et al utilized four European databases in their study that gathered data on 21,981,019 patients, with 17,699,973 registered as being adults for at least 1 year or more. The four databases used were the Health Search Database (HSD) in Italy, the Integrated Primary Care Information (IPCI) in the Netherlands, The Health Improvement Network (THIN) in the UK, and the Information System for Research in Primary Care (SIDIAP) in the Catalonia region of Spain (2). Although the percentages of Mexican-origin adults will tend to be on the lower end in these areas, this study proves that lots of useful insight can be shown on a greater scale outside of the U.S. The sample studies of anonymous citizens from these countries viewed in Alexander et al’s study prove useful in establishing a baseline understanding of NAFLD’s symptoms and steps in its prevention and how databases like the ones above can emphasize any special steps in providing proper care for more negatively affected groups, such as Mexicanorigin adults.
Semantic harmonization was used to identify 176,114 patients with diagnosed NAFLD and/or NASH; represented 1% of
the population, 0.3% being from the UK, and 2.7% being from the Netherlands (2). Despite this, 2 out of the four databases were not able to provide specific codes that distinguished NAFLD from NASH, meaning only diagnoses of NASH were possible in the UK (n=1133) and in Spain (n=1887) (2). In addition to having access to a variety of different databases, it’s important for people like the researchers in the article above and the Great Lakes Research Network Institute to ensure that NAFLD and NASH are well distinguished in order to ensure that the proper access to medical and therapeutic pathways for MO adults are functional.
Conclusion
This cross sectional study of volunteers at a communitybased clinical research clinic demonstrates a high prevalence of NAFLD. However, viewing groups of patients from McAllen and Mexico over months of June 2024 to November 2024 have shown lots of insight into FibroScan’s efficacy, the genetic and healthcare disparities that Latino populations are facing, and the other investigated diagnosis and therapeutic methods. Our data on relatively high steatosis and fibrosis scores throughout the 6-month study supports the more extreme effects that fatty liver puts on Mexican-origin patients, while the slight negative correlation between CAP and kPa indicates a variety of other factors outside of steatosis that can lead to increased fibrosis.
As more diagnosis methods and therapeutic options for patients with NAFLD are constantly emerging, it’s important to recognize the wider and more accessible healthcare resources for lower-income communities. Latino communities like those we studied and scanned for in McAllen, Texas do not fall out of that box. Various genetic predispositions like the PNPLA3 I148M variant, various chronic diseases like diabetes that cause metabolic syndrome, and socioeconomic factors such as diet, exercise, and other lifestyle modifications are already prevalent throughout our
studies and others, and continue to remain targets in helping aid these patients and in fighting NAFLD. However, it’s also important to note the complex interplay between metabolic syndrome and NAFLD’s presence, which does not necessarily label lifestyle changes such as exercise and dieting as the only solutions to preventing disease. Extra steps in medical institutions need to be taken in order to properly track and prevent NAFLD’s progression. Taking steps like establishing more local health clinics for MO adults will go far in helping provide the necessary diagnostic and medical resources that are needed to take preventative measures. In addition, much of our environment outside of our own body, like exposure to certain molecules and/or chemicals, can trigger scarring in the liver or the failure of healthy blood flow in patients. This emphasizes the need for much safety in lower-income communities’ environments.
Overall, our study appears to agree with much of the available data and research surrounding NAFLD, and it’s important to note that much study on the McAllen population will be able to provide a base understanding and education for its local communities and beyond.
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