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What to Eat: Going by the Textbook Part II

My last post discussed the book It Starts with Food and the principles it's based on. Going over the post, I realized that the part about hormones raised some questions. How do cells become insulin resistant? How can too much insulin lead to weight gain? Does too much carbohydrate cause leptin resistance?

I'm looking again at the book Endocrinology: Basic and Clinical Principles by Shlomo Melmed and P. Michael Conn from 2005. The book says it isn't clear how insulin resistance develops, but says that it is a "key feature of the prediabetic 'metabolic syndrome' (central obesity, hypertension, insulin resistance, and dyslipidemia)" (page 318). It doesn't say how to reverse it.

The book does say that insulin promotes fat formation and inhibits fat burning:

Insulin promotes lipid synthesis and inhibits lipid degradation. Before insulin became available for treatment of type 1 diabetes, patients with this disease were invariably thin, reflecting the importance of insulin in lipid metabolism....Insulin increases fatty acid synthesis in the liver....Insulin inhibits triglyceride breakdown in adipose tissue...(page 318)
Why would someone have so much insulin in their bloodstream?

The main function of insulin is to lower serum glucose. (page 311)
Where does the glucose come from? The major source for most people is dietary starch and sugar. Reduce the starch and sugar intake, and you'll reduce the need for insulin.

On to leptin. The book's section on leptin begins with an interesting sentence:

Body fat stores remain very constant over time, in spite of large changes in energy intake and energy expenditure. (page 384)


It looks like they don't subscribe to the calorie balance or calories-in-calories-out school of thought of weight control. The authors state that the causes of leptin resistance are unknown, but there are probably several. Since leptin is a fairly recent discovery, I sought a more recent endo book for more information: Manual of Endocrinology and Metabolism, 4th Ed. by Norman Lavin from 2009. It states,

Leptin is a hormone secreted by fat cells and is a major regulator of adiposity....In humans, the level of leptin in the blood correlates strongly with body weight, percentage of body fat, and body mass index. Abdominal fat cells appear to produce more leptin per cell than do fat cells in the thigh. An analysis of 15-year longitudinal data from the New Mexico Process Study found that leptin levels were highly correlated with the development of insulin resistance in older persons....Current data suggest that high leptin levels are at least a marker for insulin resistance and the hyperglycemia of aging and may actually play a role in the pathogenesis of metabolic syndrome. (emphasis in original) (page 696)

In common obesity, a state of leptin resistance develops in which leptin loses its ability to inhibit energy intake and increase energy expenditure. Following weight loss, serum leptin levels fall. (page 20)

Based on these endocrinology books, high blood glucose leads to high insulin levels, which can lead to increased fat storage and decreased fat burning. If this takes the form of a spare tire, those fat cells will release a lot of leptin, which is supposed to regulate appetite, but won't if you're obese and leptin resistant. Since leptin resistance is highly correlated with insulin resistance, you'll not only have a disregulated appetite, but probably, glucose will have a harder time getting into your cells, and your body will have to make more insulin, which can add to the spare tire. The problem isn't just the unattractive spare tire, it's also high blood pressure, dislipidemia, and diabetes (metabolic syndrome).

As good as this information is, it doesn't address the reason my friend (to whom I gave It Starts with Food) got interested in elimination diets in the first place: inflammation. Most foods that are high in sugar or starch (grains, beans, and potatoes) also include lectins, gluten, saponins, or other bits that provoke autoimmune reactions in some people. Those lovely neolithic plant foods are a disaster for some of us in many ways.

Comments

Larcana said…
Very true, I use a paleo/primal therefore gluten free diet in my wound clinic to help patients heal. They frequently have high CrPs and prolonged inflammatory states. And although inflammation is essential to start healing, prolonging it stops healing.
This could be the gut/inflammation/obesity tie in. When does the high level start to compromise the system as a whole and kick it into chronic disease states (diabetes/metabolic syndromes)? Can lowering inflammation too early with ibuprofen impede healing...can prolonging it with sugar impede healing? Which is worse or can we even stop this trend at all? Great post!
Lori Miller said…
Thanks, ludicinterval. Chronic inflammation probably has much to do with healing and obesity.
Galina L. said…
After a modest weight loss of 30 lb and keeping it off for 5 years my insulin and leptine are both low. There is nothing I can do about low leptine except killing some fat sells with lipo or laser cavitation. I attempted to do the last thing and lost 2" in my middle-section. I am sorry I failed to re-check my leptine afterwards, but I hope there are less of small fat sells now to give the wrong message to my body .
JanKnitz said…
I have PCOS, and I have had severe symptoms ALWAYS. I was very thin into my mid-thirties when I started hormonal fertility treatments and then the obesity came on like gangbusters. I have a very hard time convincing health professionals that I was ever thin with a significant degree of insulin resistance.

Now my 12 year old daughter has been diagnosed with severe insulin resistance/metabolic syndrome and her BMI and body weight are exactly what they should be--not an ounce of extra fat. It seems to me that there is a genetic component to the insulin resistance, in our case at least obesity did NOT cause insulin resistance, but did eventually cause obesity for me. We also suffer from hyperandrogenism (the PCOS symptoms)--I think those, too are a result of--rather than a cause of--insulin resistance.

I don't know where we are as far as leptin. It would be particularly interesting to find out my daughter's levels.
Lori Miller said…
Yes, I think insulin resistance probably leads to obesity, not the other way around, particularly if muscle cells become insulin resistant before fat cells. It's too bad so much time and effort have been dumped down the rabbit hole of researching low-fat diets--we might have more answers on hormones and autoimmune illnesses.

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