'Why We get Sick' by Ben Bikman, PhD (review)
Insulin resistance is the underlying cause of the chronic diseases that are shortening American life expectancy
A dying America
Despite spending more than twice as much per capita on health care, life expectancy in the United States lags that of other industrialized countries — and not by a little. For example, a child born in the United Kingdom can now expect to live about four years longer than a child born in the United States, even though the UK spends less than $5,000 per person on health care, while the US spends more than $11,000 (The Global Economy, 2020)
What’s worse, American life expectancy peaked in 2014 and has recently fallen off a cliff — while comparable industrialized countries have barely declined at all (Figure 1, below).
Benjamin Bikman, PhD’s recent book Why We Get Sick (2020) helps explain how this has happened.
In the Foreword, Jason Fung, MD explains the problem:
“In 1900, the top three killers were lung infections (pneumonia or influenza), tuberculosis, and gastrointestinal infections…. .
“Today, if we ask the question, “Why do we get sick?” we get a very different answer. The top two causes of death, as well as five of the top seven causes (heart disease, cancer, cerebrovascular disease, Alzheimer;s disease, and diabetes), are related to chronic metabolic disease.” (Fung 2020, p. xi).
Our understanding of what it means to be “sick” used to be dominated by infectious diseases. Now, it is dominated by chronic, progressive disorders that have their origins in metabolism.
Insulin resistance and its association with chronic disease
The first sections of Bikman’s book describes the association between insulin resistance and the heart, brain, and reproductive health. It shows how insulin resistance promotes cancerous tumor growth, accelerates ageing, disrupts kidney function, and causes obesity. In every chapter, Bikman presents convincing evidence summarized from hundreds of scientific studies.
What he doesn’t do is spend too much time debunking outdated, unworkable theories that have failed improve American health. For example, Bikman (correctly) bypasses the now discredited cholesterol hypothesis. Although he could summarize the counter-evidence in convincing detail, Bikman sweeps it away on page 18 when he writes “there’s little consistent evidence to support the theory that LDL is as lethal as we once believed.” Instead, he suggests you monitor your triglyceride to HDL cholesterol ratio, which is associated with increased mortality from adverse cardiovascular events. Also, Bikman correctly characterizes statins as providing “remarkably little benefit” for most people.
These comments, written in plain language like the simple facts that they are, downplay the controversy that has biased other popular books on related topics. For example, Peter Attia’s more recent Outlive (2023) expounds on the esoteric details of submeasures of LDL particle size. Bikman’s superior, albeit brief, treatment leaves the reader with the impression that we should not bother with Attia.
And Bikman is correct.
Although many readers might find it difficult to believe that practically all the major causes of chronic disease have their origins in a single disorder, Bikman’s case is convincing. Insulin is a hormone that shuttles glucose from the bloodstream into human cells, where it can be converted to energy by the mitochondria. Thus, every process in the human body is guided or modulated to some extent by insulin.
The condition in which the body can no longer make insulin is called Type 1 diabetes. That was the condition in which I found my six year old son, shortly after Christmas. Unbeknownst to me, for reasons that still remains a mystery to modern medicine, the islet cells in his pancreas responsible for producing insulin had been destroyed by his own immune system. Consequently, his body became incapable of using glucose as energy.
When we admitted him to the pediatric intensive care unit, he was in a state condition called ketoacidosis that can happen in Type 1 diabetics when their body switches entirely to fat metabolism. When his doctor put him on an insulin drip, I could watch his health return to him in real-time.
My son’s experience, and that of so many other Type 1 diabetics, is proof enough that insulin is essential to the healthy functioning of the metabolism. However, Bikman isn’t writing about a deficit of insulin. His entire book is dedicated to the problem of having too much.
Ironically, the condition in which a body produces excess insulin is also called diabetes, albeit Type 2. In this condition, the cells become resistant to the action of insulin, preventing the migration of glucose from the bloodstream into the cell for mitochondrial conversion.
Thus, both Type 1 and Type 2 diabetes result in elevated blood glucose, but only Type 2 is accompanied by hyperinsulinemia — i.e., elevated insulin.
The double whammy of too much hyperglycemia (too much blood sugar) and hyperinsulinemia (too much insulin) causes havoc in the cardiovascular system. The endothelial cells, which line the inside of every blood vessel, are particularly affected. These cells lie between the bloodstream and the smooth muscle tissues that control vasoconstriction and vasodilation.
It is the endothelial cells that are responsible for signaling those smooth muscles to contract or relax to control blood flow. When the endothelial function is disrupted by aberrant blood glucose and insulin levels, they fail to control blood flow. That’s why erectile dysfunction can be one of the first signs of insulin resistance in men. An erection depends on proper functioning of endothelial cells to control the flow of blood that engorges the penis. When the endothelial cells don’t work right, neither does the penis.
If left unaddressed, the insulin resistance that causes erectile dysfunction will eventual cause dysfunction in every other vital organ of the body by disrupting the proper blood flow and metabolism of the brain, the heart, the kidneys, the liver, and practically every other function on which your body depends.
Causes of insulin resistance
The second section purports to describe several “causes” of insulin resistance, but it mostly succeeds in describing correlations. For example, insulin resistance causes obesity. But obesity also causes insulin resistance. In other words, the two are associated with one another, but it is impossible to say which really causes which.
For example, I know a woman who used to suffer from anorexia nervosa. She was a former runway model, experience body dysmorphia, and maintained only 12% body fat, which is very low for a woman — especially one in her late 30’s with five children by birth.
Despite her lean body composition, her anorexic diet consisted mostly of coca-cola and aspirin. Her 800 calorie/day diet was mostly carbohydrates. To help conceal her anorexia, she claimed to be vegetarian so that she could refuse food in public settings.
It wasn’t until her doctor discovered that her HbA1C (a measure of the frequency with which a person experienced blood glucose spikes) was in excess of 7 that she realized she had become full-on Type 2 diabetic. The combination of elevated blood glucose and elevated insulin likely drove the growth of an in operable tumor on her liver, for which she was hospitalized.
That was her real wake up call.
You might be relieved to know that she adopted a ketogenic diet, began practicing ice baths, brought her HbA1C down to healthy levels and a scan revealed that had shrunk her tumor as a result. She is now in much better health.
Nonetheless, her insulin resistance wasn’t caused by obesity, nor did obesity cause her insulin resistance
The simplest explanation for the cause of insulin resistance is excess carbohydrate intake. That can happen under conditions of both calorie deficit or calorie surplus, under a program of regular exercise, or profound lethargy.
Bikman covers genetics, hormones, obesity, chronic inflammation, oxidative stress, diet, and what he calls “life style factors” like cigarette smoking, and while I can find no flaw in any of his descriptions, the second section lacks the clarity of the first. The fact is that we don’t really know why the body responds to excess carbohydrates by becoming insulin resistant.
By personal hypothesis is that there are evolutionary origins to insulin resistance that favor protection of the mitochondria inside the cells from oxidative damage resulting from glucose overload. That is, by slowing the rate at which glucose enters the cell, the mitochondria avoid damage by glucose overload. Bikman is not so speculative as to commit his own imaginings to writing in his book. Instead he explains, “nothing I write in this book is based on my opinion, but rather published, peer-reviewed science.”
I, for one, would be interested to read some of his opinions or editorial musings. Having done the difficult work of becoming expert in the scientific literature, I think he’s earned the right to offer his opinion, and that his readers would do well to be paying attention to it. Still, his reticence does put him in the unassailable postion of being correct — at least to the extent that his entire book is well-founded by the primary source data.
What to do about insulin resistance?
The third and final section of the main text describes several interventions that can ameliorate insulin resistance. The first of these, exercise and diet, will come as no surprise to any reader.
However, it was with great interest that I read his recommendations on deliberate cold exposure — e.g., ice baths. Because I co-Founded the Morozko Forge ice bath company, I have a financial stake in presentation of the science of cold exposure and I’m pleased to see Bikman describe it favorably when he writes “Frequent exposure to cold is perhaps the most unexpected (and unpleasant) thing you can do to improve and control your insulin levels.”
Not only is it unexpected and unpleasant, but it is also extremely effective.
Bikman summarizes some of the more drastic medical interventions, including drugs and surgery, that might be suitable for extreme cases of insulin resistance. And he also provides some guidance for readers that is likely to improve their conversations with their medical doctors about their insulin levels. (Bikman, like me, is a PhD — not an MD). He includes examples of exercises and foods that will help promote healthy metabolism and improve insulin sensitivity, and for reader’s who are inspired by the earlier material to take control of their metabolic health, these guides are an outstanding place to start.
Summary
As a profession, science is only just beginning to emerge from the dangerous myths of the cholesterol hypothesis, and the fallacy that heart disease, diabetes, and dementia are all separate diseases. Bikman’s Why We Get Sick is an enormous leap forward for popularizing a better understanding of how metabolism actually works, and its critical relationship to chronic disease. When you’ve finished reading his text, you will no longer think of declining US life expectancy as some sort of tragic and mysterious inevitability. Instead, you will begin to think of yourself as an exception to the statistical rules, and be motivated to change your own lifestyle so as to avoid the a premature, medicated, and miserable truncation of your potential healthspan.
