Title: Why we get fat, How to fix insulin resistance, IGF-1 and Cancer
AMI Rating: 10 / 10
Key Takeaways: Great lesson explaining fat growth in the body and the role of insulin. Important knowledge for everybody! Ben Bikman, PhD. explains complex subjects in an easy-to-understand and entertaining way.
How do we get fat?
Fat tissues grow in two ways:
Hypertrophy: each individual fat cell gets bigger in size (but the total number of fat cells stays the same)
Hyperplasia: a proliferation of fat cells, so an increase in the absolute number of fat cells (but their individual sizes stay the same)
Hypertrophic fat cells are insulin-resistant
Resistance: insulin typically signals the fat cell to grow, but once a fat cell has reached its maximum size, it starts ignoring insulin’s orders
Leaking: insulin typically signals the cell to keep the fats locked in, but once the fat cell becomes too big and becomes insulin-resistant, it starts to leak its fats into the bloodstream; these leaked fats start forming ceramides
Spreading: ceramides start spreading in the body and accumulating in other organs such as the liver, which in turn makes these organs also insulin-resistant!
Inflammation: fat cell gets so large that its organelles can no longer get adequate blood flow (through which they get nutrients); it attempts to recruit more blood vessels via release of inflammatory hormones
Hyperplastic fat growth makes the body fat (because fat cells are multiplying), but each individual fat cell is functioning properly (remaining insulin-sensitive), and as a result, the body is considered metabolically healthy despite being obese!
Ethnic disparity: Chinese subjects experienced hypertrophic fat growth earlier than Northern European subjects in the study
How to test: high insulin and high blood pressure = pretty much means hypertrophic fat growth
What does insulin do to a fat cell?
Insulin is a hormone that helps us absorb nutrients from our food. When we eat carbs, the amount of sugar in our blood increases, and insulin is secreted by the pancreas. Insulin shuttles the sugar out of the bloodstream and into our organs, where they can be used as fuel! (source: WTF is insulin?)
EVERY cell in the body (brain, bone, etc.) has an insulin receptor
Insulin regulates the body's use of energy (use as fuel, store, expel)
In fat cells, insulin controls two processes:
Lipogenesis: the creation and storage of lipids as triglycerides
Adipogenesis: the creation of new adipose sites (this process is naturally over at the end of puberty, meaning our fat cell count is “set” at that point of early adulthood… but we keep getting fat as adults due to lifestyle choices)
A study found that 88% of US adults are metabolically unhealthy! Measured by waist circumference, blood pressure, elevated glucose, high triglyceride, low HDL; all of which are caused by insulin-resistance
What is the harm of insulin resistance?
Insulin resistance has a hand at almost every chronic (and even acute infectious) disease: type-2 diabetes, Alzheimer's, migraines, hypertension, female health like PCOS (high insulin impedes estrogen production), erectile dysfunction
What is the cause of insulin resistance: general overconsumption of food (excess calories) or the continuous consumption of foods that keep spiking insulin (hyperinsulinemia)?
When insulin is low, the body has a significantly higher metabolic rate and can burn more calories (up to 270 additional calories)
When insulin is low for an extended period of time (over 16 hours), the body can shift in metabolic fuel from sugar-burning to fat-burning
Fats are converted to ketones, some of which is used as fuel and some eliminated (via breath or urine)
What people don’t appreciate is that even when ketones are eliminated as waste, the body is functioning at a higher metabolic rate, and the fats that would have otherwise stayed in the body are being burned off!
A study showed that when healthy college-aged men were injected with insulin they developed insulin resistance at a rapid pace. This may mean that elevated levels of insulin, rather than caloric surplus, is the main culprit for insulin resistance
What are non-food drivers of hyperinsulinemia?
Chronic inflammation: studies done with people with autoimmune diseases (aka those with chronic elevated inflammation) showed the close link between inflammation and insulin resistance: rheumatoid arthritis “flare-ups” episodes correlated with insulin resistance
Stress hormones (cortisol, epinephrine) elevate blood glucose levels, which increases insulin and leads to insulin-resistance
Sleep deprivation: one night of bad sleep can lead to insulin resistance the next day
Is insulin resistance reversible?
Readily reversible: in type 2 diabetics, once they start reducing carbohydrate consumption, they become insulin-sensitive again, within about one week
What is the solution?
Why “Eat Less, Exercise More” is not the answer: hunger wins every time in a world of abundance of hyperpalatable foods. Instead, more attention needs to placed on the type of calories we are consuming (rather than the number of calories)
Advice: eat food that nourishes the body, but that doesn’t spike your insulin
IGF-1 (Insulin-like Growth Factor 1) and Cancer
IGF-1 signals anabolic pathways that stimulate growth
IGF-1 and insulin inhibit cellular regeneration (autophagy), accelerating aging
IGF-1 and protein
Some will argue to reduce protein consumption to avoid stimulating the IGF-1/mTOR protein pathway. This is unjustified. In order to grow and maintain muscle mass, we do need IGF-1/mTOR stimulation
Why you should eat proteins with fats (not with carbs): when you combine meat and carbs, you are jacking up the insulin spike (minimally from IGF-1/mTOR and largely through the insulin spike from carbs)
Cancer and insulin
IGF-1 promotes cancer growth because it stimulates anabolic pathways of cell growth
Cancer cells largely use glucose for fuel (200x the amount of normal non-cancerous cells). So, if you reduce blood glucose levels, then you could effectively starve the cancers off, aka control carbohydrate consumption
Breast tumors have 7x more insulin receptors, so hyperinsulinemia poses a particularly higher risk