Continued treatment with insulin in type 2 diabetes continues to create issues with the body, which can eventually lead to more serious diseases. It’s important to distinguish between symptoms and problems, lest we throw more fuel on the fire. Insulin is a both a signaling and a growth hormone, which causes cells such as muscle and liver to intake blood sugar, and converts circulating glucose to fat storage. Withdrawing insulin causes these fat storage depots to reduce in size and convert to ketones. Ketones are a fuel source produced from fat dissolution (lipolysis and ketogenesis).
In type 1 Diabetes, patients cannot make insulin; they must have some source of external insulin or their diet must be strictly controlled and monitored with a continuous glucose monitor. If they do not have strict control or they don’t get an external source of insulin, ketone formation gets out of control and blood sugar simultaneously rises. It causes an acute acidosis as the cells are starving and can’t translocate glucose from the blood stream to the mitochondria. The acidosis is a signal of organism impending death. This results in a life threatening diabetic ketoacidosis. Because Insulin is a fat storage hormone, Type 1 diabetics who are not yet treated with insulin are typically very thin, and when they are treated with insulin, many become overweight and develop metainflammation.
In type 2 Diabetes, patients make too much insulin and are insulin resistant. The more insulin the liver and muscle cells are exposed to, the greater the fat storage. Eventually, as insulin resistance progresses, some areas, such as hypermetabolic regions of the brain, are more resistant to insulin and the interior of those cells is deficient of a fuel source (possibly the explanation of Alzheimer’s, often referred to as Type 3 Diabetes, or diabetes of the brain). All the while, high insulin levels are causing a progressive fat deposition and high levels of circulating glucose. Adding more insulin to this metabolic fire only worsens the fire.
The symptom of Type 2 Diabetes is a high glucose, but the actual problem of Type 2 Diabetes is high insulin. Adding more insulin to a state that has high insulin is the current standard of care, and the lip service of lifestyle modification is disingenuous when dietary guidelines also promote a feeding pattern of 5-6 episodes per day, which prevents insulin receptor resensitization. Most of the industry-sponsored education is also funded by the companies who make recurring revenue from this chronic metabolic dysfunction.
In fact, there are now studies documenting that increasing insulin utilization results in increased side effects and increased body weight, consistent with the fact that insulin causes fat storage accumulation.
Approximately 10,000 years ago, human society converted from a traveling hunter-gatherer culture to a stationary farming culture, resulting in carbohydrate-rich foods (wheat, rice, corn, potatoes) becoming staples, which facilitated the expansion of regional human populations. Reliance on dietary carbohydrates as a primary fuel source was associated with a simultaneous reduction in height, bone mass, muscle mass, and longevity.
Just in the last 100 years, we observed a dramatic increase in type 2 Diabetes with the introduction of industrial seed oils, which significantly accelerated in the last 30 years, coinciding with a governmental policy shift recommending reduced saturated dietary fats. This cultural brainwash promoting a “low-fat” diet, replaced traditional fats with carbohydrates. Additionally, industry sponsored and manipulated research data promoted Omega-6 seed oil consumption as “heart healthy.”
Oxidative stress and inflammation occurs because insulin drives glucose into the liver and fat cells to the point that the mitochondria are unable to use the incoming nutrient. The cell is unable to accommodate the excessive load of glucose, and the surplus proinflammatory omega 6 fatty acids create an inflammatory cascade. Simultaneously, a nonenzymatic glycation process causes cell wall rigidity and loss of functioning surface receptors. The cell becomes resistant to the action of insulin, and external insulin supplementation only makes further insulin resistance and increases fat storage in the liver.
The triggering of Type 2 Diabetes is from excessive carbohydrates, but the maintenance of the defect is due to the proinflammatory state associated with omega 6 fatty acids from industrial seed oils. The spiraling out of control insulin resistance acts as a positive feedback loop instead of acting as a negative feedback loop, only worsening the oxidative stress. Insulin is like adding gas to a gas fire.
Insulin, the most popular pharmaceutical treatment for type 2 diabetes, was once used only sparingly in diabetes treatment, but today makes lots of money for the manufacturers. Thanks to pharmaceutical marketing and a lack of time, many physicians prescribe insulin rather than nutritional counseling or lifestyle management.
Prior to the 1920s, the mainstay of Diabetes treatment was aimed at controlling glycosuria (glycosuria occurs when the blood glucose level exceeds about 160–180 mg/dL and is easily measured). These dietary recommendations consisted of “meats, poultry, game, fish, clear soups, gelatin, eggs, butter, olive oil, coffee, tea” and contained 5% carbohydrates, 20% protein, and 75% fat. This is analogous to the Low Carbohydrate Ketogenic Diet (LCKD) . These recommendations were dramatically different from current low-fat, high-carbohydrate recommendations for patients with diabetes. Also note that the feeding frequency rarely included breakfast, and manufactured snacks were not yet invented, resulting in 2 low-level glucose spikes, as opposed to today’s 5-6 spikes. Also, vegetable oils were not routinely available before the 1940s and 1950s. .
Exogenous insulin for the treatment of Diabetes was introduced in the 1920s, which began the switch to controlling diabetes through pharmaceutical management instead of lifestyle management, to the point that many type 2 Diabetic patients now consume excessive carbohydrates knowing they can chase it with insulin. Unfortunately, these patients already have a high insulin level, and the extra insulin only makes the insulin resistance worse. Additionally, the fat storage action of insulin, makes the metainflammation worse as well as the patient’s obesity. This is like a fat dog chasing its tail. The glucose is the tail, the mouth is the insulin, and the fat dog is the metabolic derangement.
Several recent studies have re-examined the effect of carbohydrate restriction on type 2 Diabetes and revalidated the safety and efficacy of the Low Carbohydrate Ketogenic Diet (LCKD). These studies confirmed that hemoglobin A1c improved to a greater degree over one year with a low-carbohydrate diet compared with a low-fat, calorie-restricted diet. Specifically, the participants had greater improvement in glycohemoglobin while on the low-carbohydrate diet than when on a eucaloric low-fat diet. Because LCKD can be very effective at lowering blood glucose, patients on diabetes medication who use this diet should be under close medical supervision or capable of adjusting their medication.
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So, we know that patients with type 2 diabetes have the symptom of too much glucose, but their actual disease process is excessive Insulin, with the cells being insulin resistant; yet, we treat them with more insulin. This begs the question, why and who benefits? (This is in no way to be construed as suggesting insulin is bad; insulin is a lifesaving drug. It’s meant to suggest that patient therapy should be first geared to lifestyle changes, and insulin should be the rescue drug.)
Making lifestyle changes and counseling patients takes time and energy, which most healthcare providers lack. As the one of the key decision makers, physicians remain a primary focus of pharmaceutical company sales success. The pharmaceutical industry employs numerous marketing and promotional efforts to influence prescribing patterns, starting early in medical school, even in the preclinical years of study. These marketing strategies continue throughout a physicians’ career. Drug company marketing strategies include gifts and benefits ranging from low-cost gifts to expensive trips and grants, which leads to suboptimal prescribing practices and promotes more expensive medical treatment. One could postulate that most physicians are simply a marketing tool used by the pharmaceutical companies to get their products sold; they are an indirectly paid sales team.
Often, the pharmaceutical companies launder their education endeavors through patient advocacy groups that on the surface appear to be trusted authorities, such as The American Diabetes Association.
It is obvious that Big Pharma will not be likely to support studies that reduce the utilization of their products over non-compensable lifestyle changes. Evidence-based academic research is also unlikely to be performed by academicians who are funded by these same interests. The entire health delivery industry seems to be geared towards medicalization of treatment rather than lifestyle improvement, which would radically disrupt the status quo. Big Pharma is so prevalent in the academic world of policy and thought leaders that it is no longer considered a “conflict of interest” to recommend a pharmaceutical that compensated that policy or thought leader. It is now simply considered a “duality of interest.”