I'll walk you through how you can figure out which diet is perfect for you.
Diets suck, which is probably why I’ve never written a diet book and also why I think most diet books are silly marketing ploys. Why?
Simple: most diets involve a “one-size-fits-all” approach that paints an entire population with a broad nutritional brush, without taking into consideration genetic individuality, personal health history, nutrient, vitamin and minerals holes that need to be addressed, etc.
Take the currently popular “ketogenic” diet for example. This very high-fat, very low-carb diet is championed by enthusiasts as the perfect way to lose weight, enhance cognition, increase endurance and beyond. And it does indeed work for these goals (for enhanced endurance, I personally followed a strict ketogenic diet for years while racing Ironman triathlon, and occasionally use ketosis as a brain-boosting strategy on mentally difficult days).
But when reviewing the bloodwork and biomarkers on the lab tests of my clients and people for which I do health and nutrition consults - notably people who are following one of these ketogenic diets - I’ve witnessed concerningly high levels of LDL cholesterol (skyrocketing over 400), along with high triglycerides (which can be a risk factor for heart disease and serious liver issues) and high inflammation. How could this be?
Basically, there is a condition called “familial hypercholesteremia” (HeFH) – that affects up to 10% of people worldwide. People with this condition tend to experience a metabolic firestorm in response to a high-fat diet because their cholesterol and inflammatory markers increase dramatically in response to foods such as coconut oil, butter, fatty fish and meats, eggs, etc.
As my friend and former podcast guest Chris Masterjohn has written and podcasted about himself here, the best way to get to the root of the problem in HeFH is to take the one gene for the LDL receptor responsible for contributing to this condition and try to bring it up to the expression level that would be found in someone without HeFH. How is this done? From a scientific standpoint, it can be accomplished by maximizing the biological activity of thyroid hormone and by maximally suppressing the activity of a gene called PCSK9, which is done by increasing insulin signaling. In brief, from a dietary management standpoint (and much to the chagrin of ketogenic zealots), this all comes down to eating a low-fat, fiber-rich, high-carbohydrate diet and replacing saturated fat with polyunsaturated fat - using a diet very similar to an ancestral Kitavan islander diet rich in fiber-dense carbohydrate such as coconut meat, starchy tubers, and fresh fruit.
Another example of the same dietary advice not being be good for everyone (and one big reason why, despite the prevalence of diet books, we have failed so miserably at controlling the obesity epidemic), is the wild variation in blood sugar response that can occur when subjects in controlled dietary studies eat foods like cookies, bananas, sushi and whole-grain bread. The latest research on this newly observed phenomenon suggests that each person’s capacity to extract energy from foods differs dramatically because the interactions among one’s genes, microbiome, diet, environment and lifestyle are so infinitely complex, and also suggests that common measurements of the sugar content of foods, such as the glycemic index, may be relatively useless when compared to looking at individualized blood sugar responses to foods.
One recent six-month study, funded by the European Union and called Food4Me investigated 1,500 participants in seven European countries who were randomly given personalized dietary advice based on their genetic data, or instead told to follow standard dietary prescriptions like such as eating lots of fruits and vegetables, lean meats and whole grains. Those who were in the personalized diet cohort fared far better than those in the one-size-fits-all diet group, making the researchers pretty confident that personalized diets are the way forward.