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May 11 - July 6, 2020
Ideally, and throughout our history, the ratio of omega-3 to omega-6 within our bodies would have been between 1:1 and 1:4 (i.e. four times more omega-6 compared to omega-3). If we go back to hunter-gatherer times, when all foods were fresh and the diet was not based on grains or vegetable oils, we would see this range. People living in remote areas of the world today, who consume natural home-grown foods, will have these levels as well. But if you consume a Western diet, as we have seen, many omega-3s have been removed and large amounts of omega-6 have been added to foods that have been
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The Story of the Omega Brothers
Analogy #3
We learned that the omegas originate from different parts of the plants: omega-3 from their green leaves, and omega-6 from their seeds.
The Functions of the Omega Fatty Acids
If the omega-6 to omega-3 ratio goes up dramatically, it could make our immune systems hypersensitive.
An important change in cellular walls with high omega-6 to omega-3 ratios is a decrease in the sensitivity of the cell wall to insulin in muscles and leptin in the brain. Higher insulin levels and leptin resistance raise the weight set-point, increasing the risk of obesity.7
The omega-6 fatty acids act as precursors to endocannabinoids, which are signalling molecules that stimulate the cannabinoid receptors located in the brain. Yes, you may have guessed, these are the same receptors that are triggered when cannabis, or weed, is smoked! The effect of stimulating the cannabinoid receptor when you smoke weed is an elevated, happy mood. If the dose is high enough, you are likely to experience feelings of euphoria as well. We also know what happens about an hour after the weed has stimulated those cannabinoid receptors: a sudden appetite combined with food-seeking
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Let’s look at the proven effects of high omega-6 to omega-3 ratios on the function of the endocannabinoid system and therefore on our behaviour and health.9
Activation of CB1 (cannabis) receptors leads to increased appetite and calorie intake.
Cannabis receptor blocking drug rimonobant
Activation of the system enhances sweet taste and also an increase in the release of pleasure and reward (dopamine) chemicals in the brain. Food tastes better and gives you more pleasure.
Weed similar effect
The more omega-6 in the cell wall, the more the appetite and weight-regulating system will be ratcheted towards weight gain.
Might be the reason why healthy eating decreaed my appettite
That familiar KFC family bucket craving doesn’t come from nowhere: it comes from the previous experience of KFC, whose omega-6 is still clogging up your cells and turning out cannabinoids.
Why we want dirty foods suddenly
John Stein, Emeritus Professor of Physiology at the University of Oxford, commented on the increasing ratio of omega-6 to omega-3 fatty acids, saying: ‘The human brain is changing in a way that is as serious as climate change threatens to be.’
Finally, as if the news was not bad enough already, high levels of omega-6 can prevent the body from converting the omega-3 that we get from plants to the more active omega-3 that we get from fish and animals. In other words, if the diet is already very high in omega-6 it doesn’t matter how many green vegetables you eat – their conversion into useful omega-3 will be blocked. So we have a compelling argument that, yes, a deficiency of an essential dietary nutrient – omega-3 – is a cause of obesity. This fits in with:
Read below for the proof
Figure 9.10 Link between the intake of vegetable oils and obesity rates in the USA, 1970–2010
Examples from nature may provide clues as to how our own omega messaging service evolved,
How omega ratio in nature and animals is changed over seaons naturally
According to this theory, the changes we see in response to high omega-6 to omega-3 ratios are in fact primordial protective responses against a future harsh environment.
High omega 6-3 ratio leads to survival (biological) responses
All these biological responses, which may be part of our ancient evolutionary baggage, if present, were designed to help our survival. In that case, then, a major cause of obesity is not a lack of willpower, or laziness, but the appropriately protective weight-gain response to a change in the environment.
Summary
And the amount (or ratio) of the two fats on our cell walls has profound effects on our metabolism, our weight and the degree of inflammation within our bodies.
Increased cellular omega-6 levels cause an increase in inflammation (contributing to a range of Western diseases). Increased inflammation (via TNF-alpha) leads to poorer functioning of insulin and a dulling of the effect of leptin (the hormone produced by fat cells that keeps us thin). Poorer insulin function means that more insulin is required within the blood. Higher levels of insulin also result in a dulling of the leptin signal. All these effects result in a rise in the weight set-point and then, inevitably … weight gain.
There is some evidence that the foods that hibernating animals eat before winter sets in act as a trigger for rapid weight gain. The signal comes from the shift of food availability in the autumn/winter towards nuts and grains (omega-6) and away from shoots and leaves (omega-3) – affecting the animal’s cellular omega-6 to omega-3 ratio and triggering weight gain.
Just like the deficiency diseases of the past – beriberi and scurvy – could a relative shortage of omega-3, compared to omega-6, be an important trigger for today’s health epidemic – obesity?
Insulin causes blood sugar to be stored in cells to be used later. Normally it is produced by the pancreas gland in response to a high level of glucose in the blood.
Insulin is a great drug for getting glucose into the muscle cells if you are an athlete.
Taken together with sugar to pump it into muscle cells
High insulin = higher weight set-point Lower insulin = lower weight set-point
As we learned in chapter 3, insulin causes the master controller of our weight – leptin, the hormone produced from our fat – to malfunction.
The metabolic effects of leptin resistance (in this case caused by high insulin levels) are the same as if leptin levels had been reduced by weight loss from an illness or a famine (or a diet): low metabolic rate.
Insulin ➞ leptin resistance ➞ lower metabolism ➞ higher weight set-point
Decreasing insulin level ➞ decreased weight
If there is too much unfriendly omega-6 in the cell membrane (because of excessive vegetable oil and grains in the diet), then insulin won’t signal properly. You will need to produce more of it to get the same effect.
Insulin resistance
Western diet ➞ high omega-6 to omega-3 ratio ➞ insulin resistance ➞ more insulin ➞ higher weight set-point
More insulin needed to signal properly
A Teaspoon of Sugar …
Read all to understand how insulin works
Our brain needs sugar – it needs the glucose in our bloodstream to function.
In starvation - fat molecules are used - keton bodies generated
When insulin levels are high, the body switches to storage mode: insulin forces glucose from the blood and into fat cells, where it is converted to triglycerides.
Trilycerides increases the risk of heart disease
As an example, a teaspoonful of sugar contains 4.2g of sugar – the same amount as in one eighth of a can of Coke, and the same amount contained in four sticks of celery.
The total amount of insulin produced to deal with the Coke sugar would be exactly the same as the total amount of insulin required to deal with the celery.
Much slower secretion of insulin when eating celery
The insulin works to open up the fat cells to suck the sugar into them but …
By eating so much highly processed food, and with the new culture of satisfying ourselves during the day on snacks, we are increasing the total amount of insulin that is required to cope with these waves of glucose.
Higher than average insulin levels over several weeks will increase your set-point, and weight gain will follow. Whereas lower than average insulin levels over several weeks will lower your set-point and effortless weight loss will follow.
So it is not about the total number of calories that we are consuming with our constant snacking – if these calories counted as part of an energy in/out equation we would quickly balloon to 200kg, and remember that the massive increase in the number of calories that we are consuming in our sugary snacks is burned off by ratcheting up our metabolic afterburners. This is our normal metabolic adaptation to over-eating (as discussed in chapters 1 and 3). The crucial point – which contributes to people gaining weight – is the effect of insulin on the weight set-point. Insulin dulls the leptin
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But this book is all about not counting calories and instead questioning how different factors affect us metabolically.
They found that in heavy drinkers a cellular mechanism occurring in the liver seemed to be able to literally burn alcohol calories, creating increased thermal energy (in a similar way to the thermogenesis described in chapter 3).fn4 Subsequent
Microsomal ethanol oxidizing system
These studies explain this phenomenon. In heavy drinkers, alcohol is broken down and converted, not to chemical energy to be used or stored in the body, but to heat energy which is radiated through the skin. This is the reason a heavy drinker, during an alcohol binge, will not feel the cold, even in sub-zero conditions.
How is alcohol energy processed in most of us? Alcohol energy itself cannot be stored in the body in the same way that fat or carbohydrates can be. The body treats it like a poison, breaking it down first into a chemical called acetaldehyde (which causes your hangover) and then into acetate (vinegar’s essential component), before finally being converted to carbon dioxide and water. During the breaking down of alcohol, small particles of nicotinamide adenine dinucleotide (NADH) are released. These particles contain the energy to charge up those ATP micro-batteries (discussed in chapter 7) in
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Alcohol metabolism until fatty liver
On that basis, there does not seem to be a compelling link between alcohol and weight.
One explanation for this could be the effect that alcohol has on the steroid hormone cortisol. We now know that alcohol causes higher levels of cortisol to be produced.8
Cortisol causes changes in the ditribution of fat in the body
But the side effect of this is that when we drink alcohol it can lead to lower levels of blood sugar. The brain senses this and tells us to go and eat – producing the late-night craving for an after-drink kebab, or the early-morning need for a fry-up.
The people of the Baltics, Eastern Europe, Russia, France and South Korea have not yet fully embraced highly processed Western foods, so despite their high alcohol consumption, even when they do over-eat it is with foods that do not raise the weight set-point.
If the calories in alcohol are not stored, then how do we explain the common observation that people lose weight when they stop drinking? They tend to be people who drank quite heavily before quitting. When they stop drinking alcohol, their appetite returns to normal, and their eating behaviour improves. This, combined with a drop in their cortisol levels, leads to a decrease in their weight set-point and subsequent weight loss.
