Welcome


My name is Gina and I would like to welcome you to my blog!

On this blog, I not only share the dietary and lifestyle approach which reversed my metabolic disease and achieved my weight loss, but I also debunk many misconceptions surrounding obesity and its treatment.

I am 5'5" and was weighing 300 lbs., at my heaviest. I lost a total of 180 lbs. I went through several phases of low carbohydrate dieting, until I found what worked best and that is what I share on this blog. Once on a carbohydrate restricted diet, along with intermittent fasting, I dropped all of the weight in a little over two years time.

My weight loss was achieved without any kind of surgery, bariatric or cosmetic. I also did not take any weight loss medications or supplements. I did not use any weight loss program. This weight loss was solely the result of a very low carbohydrate, whole foods based diet, along with daily intermittent fasting and exercise.

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Sep 23, 2019

Six common beliefs addressed, Part 39

1. If you are following your diet, there is no reason to not reach "goal weight".

Your fat cells are responsible for releasing leptin. Leptin is a protein that acts as a hormone, mainly through the signaling of nutrient/energy stores to the brain. This helps regulate appetite, metabolic rate and fat storage.

When you lose/shrink fat cells, you lose leptin. Therefore, fewer fat cells = less leptin. This occurs to everyone. It's a natural response, by the body, when it loses weight, any weight, that results in less body fat. For the body, the loss of body fat always equates to starvation, regardless of whether it makes sense to us or not. We know that we aren't truly starving, but the body doesn't care what you know. As far as the body is concerned, the trigger is simple - loss/shrinking of fat cells = starvation. Period. There is zero negotiation with this fact. Zero.

When the body senses starvation it puts into motion a process that results in every dieter's sabotage, but has specific unique implications for the obese - the body tries to stop fat loss. It does this by downregulating leptin expression, most likely at the leptin receptors in the brain, but no one yet knows for sure the exact mechanism. This downregulation of leptin expression, from the direct result of fewer fat cells, is the reason why it is so difficult to lose enough weight and maintain it off. Leptin downregulation is an anti-starvation effect that always kicks in and no one has been able to successfully stop from occurring. Only exogenous administration of leptin (leptin replacement therapy) has counteracted it, but this is only done in a research setting.

As you can see, because weight gain and loss is at the discretion of your neuroendocrine system, simply following a "diet" is not the only factor that determines your weight.

2. If an obese person stops losing weight, before they are lean, it's because they are not being compliant with their diet. 

In obesity, the leptin effect is detrimental. Normally, a drop in leptin expression should occur when you start getting below the body's personal fat threshold, in order to prevent the loss of too much body fat, but for many obese people, this drop in leptin begins much earlier than it should, keeping them stuck at 'still overweight' and nowhere near lean. This is because obese people usually have a confounding problem known as "leptin resistance" and this "resistance" does not necessarily correlate with leptin levels. In fact, this problem can be better described as poor leptin expression, rather than resistance, since it can occur even with normal or low leptin levels.

Poor leptin expression, for the obese, is the result of decades of chronic disruption in proper blood glucose control resulting in insulin over expression/poor function which may or may not include  hyperinsulinemia. This results in metabolism going into starvation mode, much earlier than it should. Starvation mode in the context of still having large amounts of body fat to lose is well, no bueno. This is why obesity is much more complicated than your diet coach's insistence to just "lose the damn fat", as your body has to first allow for fat to be lost.

Chronic insulin dysfunction results in the body losing its ability to signal nutrient and energy stores properly, to the brain, and causing a high weight set point. This has no easy fix, since it's not very clear exactly how this occurs and the many factors involved in its cause. The only thing that is well known, is the end result: high fat mass = metabolic dysfunction = higher fat mass = more metabolic dysfunction. A vicious circle.

To confound the issue further, cell nutrient and energy signaling is not only dependent on leptin. Excess ceramides also interfere in this signaling process. I am sure that as obesity research continues fine tuning, we will find more and more culprits, within this signaling pathway, to blame. But, right now, leptin holds the title of - Master of Weight Set Point.

If you lose proper leptin expression, before becoming lean, you will continue to be obese. Worse, you will also continue having certain metabolic abnormalities that promote more obesity, such as hyperglucagonemia, as leptin also regulates glucagon. Leptin only responds to long term nutrient availability and energy flux. It does not fix itself overnight. This can be problematic, as most people seem to be unable to adhere to a proper lifestyle intervention for more than a month at a time. That's a problem, since long term is key, when it comes to leptin regulation.

3. If you can "hack" leptin, you can fix obesity. 

Through the years, many people have tried to "hack" leptin. Remember the - "Divide your meals into several small ones, rather than one large one." - advice? That's a leptin hack. Leptin is a starvation hormone and responds strongly to nutrient availability. Remember the - "I ate carbohydrates and my weight dropped!" - claim? That's a leptin hack. Carbohydrates raise blood glucose and decrease ketones, giving a strong signal, to the body, that it is not starving, but rather it's in surplus. What does leptin do when there is a surplus in nutrients and energy? It allows the body to burn fat and reduce weight. This is particularly true after long term starvation protocols like chronic caloric restriction. These protocols gave rise to crazy fad diets, we have seen plastered all over tabloids, which make claims like - "Eat yourself slim!" - or - "I lost weight by eating more!"

The issue with these tactics is that the temporary positive effect, they have on leptin, is counteracted by the long term negative effect they have on insulin. Leptin, as are all other metabolic hormones, is a slave to insulin. Insulin is a signal that there is nutrient/energy availability and this causes for leptin to respond by allowing fat cells to burn energy. But, if insulin starts functioning abnormally, leptin loses its proper expression. It becomes "insulin resistant". In other words, the body develops the dreaded leptin resistance, described above.

Insulin is very easy to manipulate through blood glucose homeostasis. So, "eating yourself slim" or "adding more carbohydrates to drop weight" only ends up affecting your blood glucose control which in turn will have a negative effect on insulin and eventually affect leptin.   

So, leptin is a double edged sword that works very closely with insulin. Insulin must be at normal levels and maintain a pulsatile response, for leptin to work properly. This is why it is impossible to "balance energy" with calories. There is a very complex interplay between hormones, that humans can't control by simply manipulating their calories, as insulin responds differently to different macronutrients and leptin responds counterintuitively to energy surplus.

4. There is nothing that can be done for leptin resistance.

Just because manipulating leptin is difficult, doesn't mean that you can't do some things to try and mitigate it. After all, there are real ways of controlling it, which aren't based on BS. You can help the body respond more favorably to weight loss by:
  • Having consistent meal times that aren't spaced too far apart. Following predictable circadian rhythms is vital for leptin to work properly, as there is an interplay between dopamine and leptin.
  • Normalizing insulin levels and making sure that your HbA1C matches up with your glucose readings. Losing some weight is not enough if you continue having abnormal metabolic function.
  • Avoiding 'one meal a day' (OMAD) protocols and any chronic, extended fasting. Leptin is a starvation hormone, so you don't want to give the body any signals that it is starving, in any way.
  • Allowing the body to go in and out of ketosis naturally and not forcing it to maintain chronic ketosis artificially. Chronic ketone presence is a signal, to the body, that it is starving.
  • Not restricting protein. Insufficient protein is another strong starvation signal to the body.
  • Not consuming excess dietary fat. Burning of body fat will not increase, with dietary fat intake, when there isn't proper leptin expression. Eating dietary fat will only make you fatter, if you have leptin problems, especially in the presence of growth hormone and low protein intake, which occurs with many "fad keto" and "fad fasting" protocols.
5. Weight stalls can only be caused by leptin resistance.

Leptin is the biological reason for plateaus. This is why you can be diligently following a diet and still experience a plateau. The type of diet makes no difference. This leptin effect occurs with every diet on the planet, from caloric restriction to bariatric surgery and everything in between. Remember, it occurs from anything that causes loss of body fat, so any weight loss is the trigger, regardless of the method.

Having said that, there are certain behavioral reasons for plateaus, which fall outside of leptin. For instance, disordered eating habits and obesogenic practices can cause pseudo plateaus. The reason these plateaus are described as "pseudo" is because they aren't true plateaus, as true plateaus are caused by leptin. But, the plateaus that these people experience, are primarily the result of their failed dietary protocols.

6. Obesogenic behaviors occur because of high carbohydrate diets.

I know the low carbohydrate crowd wants to insist that "carbs are what cause cravings!", but we know that's not entirely true, since we see what occurs when they follow low carbohydrate diets. Guess what? Nothing changes. Their "cravings" stay the same. These people suffer from specific behavioral issues that are manifested in their eating habits. Disordered eating and obesogenic practices are problems that are not the result of any specific diet alone and go well beyond dietary interventions.
  • Disordered eating practices: The person who believes they can eat packages of cheese, an entire bottle of mayonnaise, bottles of almond butter, tubs of coconut oil, a carton of cream and a side of bison because, you know, it’s "low carb". When they were on high carb it was boxes of cereals and loaves of bread.
  • Obesogenic practices: The person who continues to eat and drink out of meal times (snacking). They also insist on creating low carb/keto junk food, going on temporary "fad" diets for "quick weight loss", replacing protein with fat, refusing to sustain an exercise regimen and/or continuously dropping carbohydrate restriction periodically.
The people who suffer from these behavioral issues, will continue displaying them regardless of the diet followed. In fact, these are the people who are most likely to be "serial dieters". They continuously hop from one diet to the next, assuming that it's the diets that aren't working, but the only thing that isn't working is their relationship with food. By the time these people "get it together" and find a proper diet, that's not a fad, they have intractable obesity from years of yo-yo and crash dieting. They are now experiencing hypothalamic damage and their leptin simply is unable to communicate with their brain, anymore. These people will end up requiring bariatric surgery or some other extreme intervention to try and get their leptin signaling back.

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