Weight Set Point

Weight stalls are many times subjective, so in this post I will talk about legitimate weight stalls. In other words, this is for people who were morbidly obese and are now stuck at obese or overweight, not for people who are 10 - 20 lbs. from goal weight. If you are already thin and are trying to lose vanity weight or sustain maintenance, you can do so through training and simple caloric restriction. The information I am going to give here is specifically for the obese, as obesity is the focus of this blog.

The 'weight set point' hypothesis, though heavily debated, is not contested in obesity research, because of the numerous studies which have consistently shown it to be a real phenomenon. The debate primarily lies in differing opinions as to what "sets" it and what keeps it set. This varies depending on what hypothesis of obesity is being ascribed to, but the overwhelming consensus is that leptin expression is the main driver of weight set point.

Weight set point is determined by the communication between leptin, your fat cells and your brain. Leptin communicates how much stored fat you have and at what rate it's being used. It is the body's weight thermostat and it is controlled through various mechanisms including blood glucose regulation and insulin function. Two abnormalities occur in high weight set points and each one is a direct result of the other:

1. Blood Glucose Dysregulation - Chronic, erratic blood glucose levels, with large disparities between highs (postprandial) and lows (fasting) trigger the metabolic adaptation that will end in type II diabetes as it deteriorates insulin function. 
2. Chronically High Insulin (Hyperinsulinemia) - When insulin function deteriorates, it becomes overexpressed causing a condition called hyperinsulinemia. This interferes with leptin signaling, in the central nervous system, and causes fat mass to remain set to high. This causes for the body to fight to preserve its fat mass, at this higher weight set point, regardless of the person's efforts to lower it or their current state of obesity. Even a trivial amount of fat loss is enough to trigger a doubling down of leptin under expression.

There is debate in the literature as to the sequence of events in this pathology. Some believe the problem lies primarily in leptin, some in the fat cells, some in the brain itself and others in everything in between. Many different hypothesis exist to explain how any one of these three problems occur. There is even one hypothesis which is interesting, if not far reaching, as it makes the claim that the brain is purposely setting a higher weight set point in order to preserve the dopamine release it receives from "junk food" consumption. In other words - addiction. The brain is allowing you to consume more "drugs" in the form of highly palatable junk food by setting a higher weight set point. Interesting, possible, but who knows. That's Big Pharma's new problem to tackle.

As far as you're concerned, whatever the reason and whatever came first, the result is the same. The body is having a starvation response, when it shouldn't be having one, as it still has plenty of fat mass and is far from starving. The communication with leptin has obviously broken down, at some level. What is actually stored, is not being communicated to the brain, so it's not being burned and even further storage occurs instead.

Leptin controls many metabolic functions that influence fat mass growth and metabolic rate, all of which influence your weight set point:

• When there is no leptin communication in the brain, thyrotropin-releasing hormone (TRH) is deficient and thyroid stimulating hormone (TSH) is decreased. Though your TSH levels appear to be normal, the thyroid is being inhibited. This causes abnormal thyroid activity, which slows down metabolic function.
• When leptin is low, cortisol levels increase. This means more glucose release and more fat mass growth. Cortisol also further inhibits leptin function.
• Leptin controls the livers glucose production through the regulation of glucagon. Low leptin further dysregulates glucagon, which means more exaggerated glucose dumping, by the liver, and further fat mass growth.
• Low leptin levels affect the sympathetic nervous system, preventing the conversion of thyroxine (T4) to triiodothyronine (T3) and increasing the production of reverse T3 (RT3), which opposes thyroid hormones. This causes hunger, low blood glucose and inability to burn fat.
• Leptin, like insulin, regulates basal dopamine synthesis. If dopamine is being inhibited, it prevents proper glucose regulation and triggers metabolic slow down, as dopamine is a very important signaler of food availability. Dopamine allows metabolism to adapt to its environment and changes in the seasons/temperature, regulating metabolic rate.

More than likely, the miscommunication in leptin signaling is caused, primarily, by poor insulin function (insulin resistance). Overexpression of insulin causes a metabolism that is set to conserve energy, not burn it, as all obesity is mitigated through insulin receptors at the fat tissue. Insulin resistance is always greater at the muscle and liver, than at the fat mass.

If there is extreme insulin sensitivity of the fat mass and resistance in other tissues and organs, it affects leptin/adiponectin levels at the fat cell, causing dysregulation of energy flux (fuel going in and out of cells). The cells may be full beyond capacity, but they continue to signal they are empty due to insulin's action on them. This causes an even further under expression of leptin to any weight loss, even when the person remains obese, since storage signals are completely mismatched. This kind of makes sense, since storage signals must be dysfunctional for the body to allow such a large amount of fat storage in the first place. This means metabolism has malfunctioned in weight gain and will continue to malfunction in weight loss.

It seems unfair that after adopting a new lifestyle, following it diligently and losing weight, the person is left half way to their goal, with no solution in sight, but that is exactly what occurs. The body actively fights to defend its fat mass, even if it's in excess. What makes it more unfair is that the weight loss itself, is what triggers the weight stall.

When fat cells are releasing fat, instead of up taking fat, they will normally stop making leptin. The very hormone you need, and was already under expressed, is the very one that lowers with treatment. You can't completely blame the body for doing this. Leptin is a "starvation hormone", after all, and when too much fat is being released from fat cells, it technically signals panic to the body, particularly if the body is already under a starvation adaptation. The body will then react by lowering leptin, the very hormone, that causes the release of fat. The person has under expressed leptin as it is, so further lowering of leptin only makes their situation worse, at least in the short term.

You might think you have a new problem, on your hands now, but don't despair. It's this lower leptin that will eventually help you succeed with your weight loss. After all, lower leptin will break your resistance to it and enhance its expression. If you can regulate your leptin, you will have a more beneficial leptin/adiponectin ratio, causing for a healthier and more responsive fat mass.

In the meantime, the desperate person, going through their weight stall, might turn to extreme interventions, in order to force the body to lower its weight. This is done by trying crash diets and hack diets, which all use starvation as their primary intervention. But, it will all be to no avail. The weight might temporarily go down, but immediately go right back up again. Worse, these interventions will only make the problem worse, as they cause a greater leptin/adiponectin mismatch and the body will become better at getting fatter. An obese person's hormonal profile and fat mass is already primed for getting fat, it surely does not need more help doing so.

Unlike insulin, leptin only responds to long term energy input. This means that it does not correct itself overnight. It can take months to years to obtain adequate leptin expression and each time you change your protocol, you reset this process all over again. This is why chronic, yo-yo dieting eventually causes metabolism to break and obesity becomes intractable. At that point there is no protocol extreme enough to reset leptin again, aside from exogenous administration of leptin which is only done in an obesity research setting.

The best way to address a weight stall and lower your weight set point is by addressing the following issues:

Improve insulin function - The best way to keep your insulin functioning properly is to control your blood glucose. Avoid blood glucose disparities. It is poor blood glucose regulation that eventually deteriorates insulin function and leads to type II diabetes. 

Insulin is a master metabolic hormone that regulates all other hormones. Dysregulated insulin, means dysregulated leptin, dopamine, ghrelin, incretins, glucagon, estrogen, etc., since most of these hormones are insulin's slaves. Insulin is also the easiest hormone to manipulate through diet and exercise. Though insulin level alone, is not responsible for obesity (insulin function is of vital importance), it is a great place to start for taking control of your metabolic state.

Even though insulin function is not dependent on its serum levels, insulin levels can still be useful to know, particularly during the start of your dietary changes. Fasting insulin should preferably be below 3, for active weight loss, and below 6 for maintenance. If your dietary protocol is not addressing insulin levels properly, then you have to find one that does. Insulin level and regulation is primarily determined by the macronutrient composition on your plate because that's what affects blood glucose regulation.

Lower your triglycerides - Lower triglyceride levels help improve leptin sensitivity.

Triglycerides are lowered dramatically through carbohydrate restriction, because excess glucose is no longer being turned into fat. But, if your triglycerides are still above normal or higher than they should be, even on a very low carbohydrate diet, then you have to dial down dietary fat intake and get to moving, as exercise is a huge factor in lower triglyceride levels.

There are some people who have higher triglyceride levels regardless of their carbohydrate or fat intake. They have a genetic predisposition to having higher triglycerides. For these people, an entirely different dietary approach might be more beneficial.

Stick to one protocol - Don't flip flop. If your protocol has brought you this far, stick with it. You can tweak it and make small changes, here and there, but do not make drastic changes to your macronutrients, unless everything is going down hill. A weight stall is not enough to indicate a protocol is not working, as stalling occurs with all weight loss interventions.

The body's hormones require consistency and leptin only responds to what's consistent in the long term. Make sure you are getting consistent nutrients and energy.

Do not go extreme (No "hacking" or fooling around) - All this dietary "hacking" BS is just that, BS. If a protocol works, it works with no "hacking" required. If it doesn't work, then it has to go to the scrap yard, because no amount of "hacking" will make it work.

Do not attempt starvation protocols to "beat" your thermostat into submission. Beating it won't make it comply, it will only break it. You can't beat the body to do your bidding. The body is the one who delivers the beatings and it always wins. Each battle, with your body, tells you something very important -- "The beatings shall continue until morale improves."

Get adequate amounts of protein - Protein is the main macronutrient that signals to the body that you are not starving. It is the antidote to starvation. 

Protein is what's missing in every failing protocol, from caloric restriction, to extended fasting, to badly formulated ketogenic diets and to diabetes producing plant based, "low fat" diets. Protein, protein, protein. Prioritize protein. It's the most important piece of the puzzle.

Lower your dietary fat intake - You should have no less than 50 grams of dietary fat a day, but make sure you are not going over 150 grams a day. Fat intake is gauged by the fat on your body. Too much body fat = less dietary fat. Too little body fat = more dietary fat.

Get moving - If there is not enough energy flux occurring in your fat mass, it will just sit there, stalled. You must improve leptin/adiponectin signaling, to the brain, by getting up from the chair and following an exercise regimen you enjoy and can sustain. Exercise regimens must be consistent and occur daily. You are better off having some movement daily, than having a lot of movement, once a week or once a month.

Lifestyle changes. Not hacks, not temporary protocols. Obesity can only be addressed with long term solutions. Diet is long term and so it must be adhered to for life. Everything else is short term and so it's a waste of time.

Carbohydrate restriction is the best line of defense when it comes to improvement of leptin sensitivity, through the sustainment of blood glucose regulation which profoundly impacts insulin. Better leptin signaling means better communication of fat stores, reducing the weight set point.