Why you shouldn’t follow your friends successful diet
I get it. You just want to follow a successful diet.
One that will work!
I mean it shouldn’t be that complicated right? Your friend lost so much weight or resolved their health conditions following a”_____” diet. It should work for you too.
Plus, what if it’s the one diet that will finally work?
Yet, to date, there is only one “diet” that has been found helpful across broad populations. The Mediterranean diet. Which in the eyes of some is still debatable.
Not a…
- Keto
- Paleo
- DASH
- Intermittent fasting
- Weight watchers
- Atkins
- Whole 30
- Vegan
- Vegetarian
- Carnivore
- Bariatric
- High-protein
- High-protein, low carb
- Low FODMAP, etc…
And my guess is, the Mediterranean diet wasn’t the “successful diet” your friend followed.
To clarify, I’m not against following a “diet”. I mean I am a Registered Dietitian. I help guide you through food choices for better health. In fact, there are many health conditions that require a specific diet in order to heal. Or just get your health back in line.
Not to mention, some of you may need to follow a very specific diet for life just to manage your health. And that’s ok.
But what I want to show you is that just because your friend was successful with a specific diet doesn’t mean you will. Nor should you just “try it” to be sure.
Although this conversation isn’t about weight loss, this discussion is truly about how your diet influences genetics that translates into your health success. Including weight loss.
I want to dig into a couple of studies….
2022 “Polymorphisms, diet and nutrigenomics”
These studies will bring to light why just one diet doesn’t work for mass populations. And why getting consistent results have been difficult.
Now I do believe there are food components of a diet that will help mass populations. Just not one singular diet for everyone to follow.
First I want to very simply describe a few terms…
Nutrigenetics- how vitamins & minerals influence your genes.
Nutrigenomics- how your diet influences gene expression.
For example, diets rich in fats and sugar are associated with abnormal methylation patterns of neuropeptide genes that control food intake and could be involved in obesity development .
Moreover, deficiency of various micronutrients – like vitamin A, group B vitamins, selenium, potassium, and iron – are linked with hypermethylation of tumor suppressor genes that play a crucial role in cancer.
Not to mention, Nutritional metabolomics identifies the metabolic changes caused by specific nutrients or diets. It also involves the study of metabolism under various genetic and environmental stresses. Food components and nutrients interact and alter metabolic pathways in different ways.
Moreover, higher saturated fatty acid consumption results in a gene expression profile that is typical of glucose intolerance, liver lipid accumulation, inflammation, and increased neuropeptide expression, leading to development of obesity.
Furthermore, diets lacking folate and choline are linked with dysregulation of lipid metabolism genes, thus predisposing to non-alcoholic fatty liver disease.
Similarly, chromium deficiency induces down-regulation of insulin signaling genes, which may lead to type 2 diabetes mellitus.
Selenium, vitamin A, and vitamin B12 deficiencies increase the susceptibility to cardiovascular diseases by up-regulating lipogenic(involves the metabolic formation of fat) and pro-inflammatory genes.
So as you can see, the foods you choose on a daily basis play a significant role in your health outcomes.
But let’s go a little deeper. And compare a conventional diet recommendation to a personalized genetic based diet recommendation. Showing the differences in health outcomes.
I’m going to review the three cases from the second study listed above.
Case one:
This was a 45 year old male patient with obesity, high blood sugar and night eating syndrome. His fasting glucose was 112mg/dL. He reported body weight gain in the past 5 years despite exercising twice weekly. And difficulty in controlling his weight and appetite since adolescence. The patient also consumed branched-chain amino acid(BCAA) supplements. This was to decrease muscle soreness during resistance exercise sessions. The patient’s main goal was to lose weight and better blood sugar balance.
The conventional diet intervention was established. It was recommended he follow a diet high in fiber & carbohydrates and low in protein. Divided into three meals and three snacks. In hopes to reduce glucose peaks. He was also to take Vitamin D supplementation to improve his low level.
He followed this plan for 8 weeks and lost 6.6 pounds. No change in his HGBA1c and his fasting glucose lowered to 106.
Next a personalized lifestyle intervention was established. This was based off the results of his nutrigenetic test. The most relevant genetic information extracted from his analysis included…
- High genetic risk score for type 2 diabetes. Indicating the patient could benefit from a high-protein diet improving insulin resistance and beta-cell function.
- High genetic risk score for habitual coffee consumption, which is linked to improved glucose responses to a low-fat diet.
- High genetic risk score for elevated fasting glucose, which is associated with improved glucose metabolism when consuming a low-fat diet.
Additional informative genetic SNPs included…
- Prolonged duration of elevated melatonin levels, thus delaying breakfast might reduce the risk of developing type 2 diabetes
- Beneficial effects of a low-calorie, low-fat & low-carbohydrate diet
The patient was recommended…
- Replace resistance exercise with endurance training
- Avoid melatonin supplements
- Continue vitamin D supplementation
- Eat during timed window of 10:30am to sunset
- Follow low-carb, low-fat diet
He followed the plan for 8 weeks and lost 16.5 pounds. His fasting glucose lowered to 89. His A1c dropped 8.5 points. Additionally, the reduction in body weight resulted in remission of pre-diabetes.
Case Two:
A 54 year old male with overweight and type 2 diabetes. His goal was to reduce his fasting glucose of 155, loose weight, lower serum triglycerides & cholesterol and to control blood pressure through lifestyle changes. The patient was already exercising four times per week and claimed to be very careful with his nutritional choices.
The conventional dietary intervention recommended was…
- 2000 calorie diet (50% carbs, 20% fat, 30% protein)
- 30 gram fiber
- 3 meals and 3 snacks daily
The results were:
- Lost 8.8 pounds
- No changes in his A1c
- Fasting glucose was 145
- Marginal changes to blood pressure
The personalized lifestyle intervention was recommended. Based on the patient’s genetic profile. The most nutritionally relevant genetic information included…
- Low genetic risk score for habitual coffee consumption, associated with beneficial health outcomes following a high-fat diet.
- Genetic SNPs associated with a reduction in insulin and beta-cell function homeostatic model assessment(HOMA-B) following a high-fat diet.
- Risk for impaired blood sugar control following a high-carbohydrate consumption.
- Greater risk for type 2 diabetes and related co-morbidities when consuming diets rich in saturated fats, desserts and milk.
Patient followed for 8 weeks…
- 2000 calories(45% carbs, 35% fat, 20% protein)
- 25 grams fiber
- No changes in meal timing
- Avoid desserts and milk
The results were…
- Lost 4.4 pounds
- Fasting glucose dropped to 108
- Dropped 12 points on his blood pressure
- A1c dropped from 6.3 to 6
- Cholesterol dropped from 210 to 200
- No change in triglycerides
Case Three:
A 67 year old, normal-weight male with type 2 diabetes experienced dysregulated fasting glucose levels(122 mg/dL). The patient reported experiencing depressive symptoms which were verified by the Beck depression inventory score of 15.
The conventional dietary intervention was
- 1750 calorie diet(45% carbs, 30% fat, 25% protein)
- 30 gram fiber
- 3 meals and 3 snacks
- Vitamin D supplementation
After 8 weeks no improvements were detect in body weight, blood pressure, A1c or fasting glucose.
The personalized lifestyle intervention was recommended. Based on the patient’s genetic profile. The most informative scores included:
- The Low genetic risk score for type 2 diabetes, for which low-protein diets have been shown to improve outcomes.
- Low genetic risk score for habitual coffee intake which has been associated with improved health following a high-fat diet.
- The Low genetic risk score for elevated fasting glucose. For which a high-fat diet may improve glucose metabolism.
- Carrier with genetic SNP associate with reduced risk of hyperinsulinemia and insulin resistance upon adherence to a high Omega-3, low Omega-6 diet.
The patient was to follow for 8 weeks:
- Greek Mediterranean diet, high in Omega-3, low in Omega-6
- 1800 calories(47% carbs, 37% fat, 16% protein)
- 26 gram fiber
The results…
- Fasting glucose dropped to 112 from 122
- A1c dropped 3.6 points
- Lost 3 pounds
So as you can see, following your friends successful diet may not net you the same benefits. Equally the same, following a certain calorie level may miss important food properties that your body needs to maintain health.
Hopefully, you can see that taking a more personalized diet approach may be the missing link to achieving your health goals.
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