READERS SUMMARY: 1. How does MSG and aspartame affect you and your brain and your fat loss? 2. What do artificial sweeteners do to a human? 3. How does neuronal injury from diet, trauma, and energy depletion all tie together? 4. What about young humans? 5. What about young humans with injured brains? In part [...]
READERS SUMMARY: 1. How does energy depletion link neurodegenerative, concussions, and diet? 2. Why are diabetics more at risk for concussion and neurodegenerative diseases? 3. What is the NMDA receptor and why should I care? 4. How does the NMDA receptor work normally and in diseases like concussion to protect us? 5. How does glutamate, [...]
Today, I decided to blog about Intermittent fasting (IF). Since I wrote the Leptin FAQs, I have been bombarded with requests about IFing and how it relates to leptin signaling. I mentioned in the FAQs that I love IFing, but not when someone is LR. The reason for this is how the AMP-activated protein kinase pathway (AMPk) works. THe AMPk pathway is best described as a fuel sensor for lipid and glucose metabolism. In humans, the control of glucose homeostasis is governed by the balance between intestinal absorption and endogenous hepatic production by the liver and the uptake done in the muscles. Intermittent fasting is a behavioral modification that specifically alters feeding behavior to cause disruptions in glucose and lipid metabolism in humans. It also has specific times when exercising is done as well. When it is practiced well is can lead humans to shred body fat and really control their ability to generate muscle with workouts and re-feeds. I would strongly recommend that you take a look at the leangains protocol sometime on Martin Berkhan's site. The key question many have asked me is how does it work and why can't I do it right off the bat regardless of my leptin status. This is a loaded question with an answer that may make your head hurt but you will understand why IFing won't work if you are LR. The reason why it is counter productive in LR is the AMPk pathways requires really optimal leptin sensitivity and signaling to be occurring between the brain, liver, and muscles. At its core, when one IF's it creates a "temporary" cellular stress due to lack of food at certain times. AMPk is specifically upregulated in times of cellular stress. Some examples, are nutrient deprivation, ischemia, hypoxia, exercise, glycogen depletion and oxidative stress. When one fasts, this also counts as a cellular stressor.
What should I do before I start The Leptin Reset? Before you start, take a picture of yourself from all angles. Don't be bashful or you'll be sorry in 18-24 months. Next, weigh yourself naked. Let your significant other or a family member take this picture. Go to the store and buy a piece of clothing that does not fit you now, but will when you have met your goal. Remember, calories are important when you're LR (leptin resistant) and mean nothing once you are LS (leptin sensitive). Macronutirents count when you're LR and mean nothing when you're LS. How do I determine if I am leptin resistant? Remember, you can be LR (leptin resistant) if you're fat or skinny. If you're overweight by more than 30lbs, it is a lock you have some degree of LR. If you're underweight by 20 lbs, you are likely LR, too. If you had an eating disorder, you're likely suffering from a serious leptin issue. The easiest test is to look in the mirror. The mirror does not lie and it is really cheap. For those people who still can't be sure after peeking in the mirror, you can order some blood tests. My favorite is the HS CRP (highly sensitive C-Reactive protein) and the reverse T3 tests (but there are others). They are accurate in over 90{a7b724a0454d92c70890dedf5ec22a026af4df067c7b55aa6009b4d34d5da3c6} of cases.
So now that we examined Dr. Lustig's insulin theory of metabolic control we need to take a look at the reward tracts that are located in the human brain. These tracts have been well studied and their neurochemistry is well understood. What appears not to be as well known is how the hypocretin neurons and the leptin receptor control and modulate their activity. The key point here is that the dopaminegic tracts eloquently spoken of Dr. Guyenet's reward series are the "efferent only" path that is part of the effector arm of the leptin receptor and the hypocretin neurons. This means, in English, they are playing second fiddle to the leptin receptors and are not the dominant cause of obesity. They clearly play a major role in the neuro-circutry but they do not control obesity. They carry out the action but the orders were given by someone else. One of the reasons I had a major problem with the reward series, is because of my "day job" as a neurosurgeon. I have had the opportunity to operate on many brain tumors in the reward tracts and never have I ever seen either preoperatively or postoperatively one patient develop severe morbid obesity. If these tracts were truly dominant causes this would lead neurosurgeon and neurologists to see many patients with this problem. Well, we do not. That was a big issue for me with the theory. The second issue I had with it was that when we neurosurgeon's have patients with brain tumors involving the hypothalamus we see tremendous effects on feeding, obesity and on anorexia. This is well documented and I have personally seen this in many cases. Dr. Lustig pointed this out in his AHS 2011 talk when he showed some clinical cases of craniopharyngioma's and of hypothalamic trauma's that resulted in morbid obesity.
Continuing on in the Central leptin series we will resume in Orlando, Florida. In Orlando, Dr. Myers, went on to say, "In addition to examining the molecular details and importance of specific LRb signals, we are dissecting the regulation and function of individual populations of LRb-expressing neurons and examining the role of leptin in the development of neural circuits. By understanding the totality of leptin action in this way we hope to decipher the mechanisms by which leptin regulates the predisposition to diabetes and other aspects of the metabolic syndrome." This statement carries huge implications. He has found that not only is leptin neurons somatotopically organized in the brain, but the leptin receptor also appears to be somatotopically organized into certain regions that wire and select certain neurons in the brain that modulate all parts of the obesity physiologic response. It also appears that this organization is different in men and women at the parvo-cellular nucleus in the hypothalamus. Certain parts of the receptor control total body glycemic control, others body weight and size, and others power the para-mammillary neurons to directly control fecundity, placental growth and oocyte maturation. The receptor even codes for gender differences! Men and women really are from Mars and Venus when it comes to obesity and fat deposition, and this explains why the endocrine response is different in men and women. We have known men and women have different leptin levels as adults but did not know how or why this happens. Now we do. We now are beginning to understand why it is the case as well. It helps explain why we see can see PCOS and stubborn weight gain together and why fat is distributed differently in both sexes.
Today, we are going to cut deeper into the leptin story. We need to look at the leptin receptor because its biology will explain why studying macronutients at a dietary level just becomes a confusing mess with seemingly multiple paradoxes. I recently commented on this in Paul Jaminet's blog on August 24th 2011. The comment was very detailed but not written well so I am going to lay out the reasoning in the next few blogs. As most of you know leptin is the lynchpin in my Quilt and sits at position two. Many people might not realize how important it is for health, in sickness, and for optimal endocrine function. It is the dominant factor in obesity and this series is out to show you why this is the case based upon the data coming out of some labs who specialize in this neurobiology. This series is going to be laser like biochemistry on a 30 foot level. When we talk about this type of lab science it is very easy to lose perspective of the larger story I am trying to unveil to you. I have previously called leptin the master hormone of the brain. Remember that the brain has two ways to control things, one is direct neural wiring and the second is the control over the hormonal secretions body wide. Given these two factors, I think I may have under called it, honestly. This hormone signals the entire body's nutritional status, metabolic status, and endocrine status to the brain at all times. The brain in turn uses leptin to regulate total glycemic control, energy balance, and all neuroendocrine function in all systems in humans. This means that energy regulation is centrally controlled by our neuroendocrine system. The brain uses this hormone as an afferent and efferent signaling hormone to know precisely what is going on in our 20 trillion cells body wide. The brain does not have direct wiring to all 20 million cells because of space limitations of our cranium and our mother's vaginas. So it uses hormones and cytokines to extend its power and reach to send signals to those 20 trillion cells.
When you finally decide to take total control of you life and optimize yourself I always suggest testing. Many of you have bombarded my email and my twitter account for a blog to a list of those labs. Well, today's post is for you. I was resistant to do this because I felt having the list of labs is a waste of time if you don't have a physician who can decipher what they all mean for you. 7 years ago, I could not tell you what this group of labs meant at all to your optimal health. I learned it by reading and going to classes to optimize myself. After much reflection I have decided to give you what you asked for. I am fortunate because many of the PCP's I work with understand these tests well. I may also update it as I think it needs to be updated over time. The first set of labs are what I call the core lab set for optimization. There are other panels I add to the core lab based upon the history, physical, and the food logs I will have patients give me. This blog is meant to be a resource for you to refer back to when the need arises. Discuss these with your doctor but don't assume they will run out to order them because they may not know what all these tests will tell them. That part takes some time. I recommend starting the dialogue with your doctor to assess their willingness to help you. Most of my PCP doctors are awesome "helpers" to their patients with these issues. This requires a lot of work on the doctors part and the patients part. Do not be surprised if this is not covered by insurance. The time required to optimize someone is unreal. I know how long I spent optimizing myself 6 years ago. It was a tedious process but I was not going to give up because I believed my life depended upon it. For most people, 2-3 years you can expect the changes you want. If you are really in tough shape it may take longer but that should not deter you. I love patients who bring big challenges. They are the most appreciative patients I have had in the last 5 years. We can never settle for a C or D when an A is possible.
I was in a lounge watching the news last week and began to over hear a group of dermatologists talk about the new FDA rules set down for sunblocks that will go into effect in January of 2012. There was unanimous agreement among them all that sunlight was the source of everything that was bad in their world. One of the doctors said to another that, "no human should be out in the sun and they should just take vitamin D3 from the drug store instead of getting it from the sun." It was at that point I knew this was going to make a blog post about this. Apparently no one realizes that photosynthesis supports most of the food chain on this planet? And we are the mammal who has an energy hog in our head that needs energy. Since our skin is derived from neuro-ectoderm and we too use photosynthesis to make Vitamin D for our protection from poor electron dense foods in summer maybe we better re think this position. It is beyond me why the sun is so vilified. We could not have evolved past single cells organisms without it. We all learned that simple fact in school. But now with advanced degrees and plaques on our wall, are we going to blame all skin diseases all on the sun now? I definitely don't buy this conventional wisdom. So I decided to begin to add pieces to the immunity levee in the QUILT because of this conversation. And before we start let me be clear. It is better to get Vitamin D3 from the natural sources before a supplement in my opinion. But there is a catch to this pearl of wisdom. First, review this link on natural Vitamin D production.
READERS SUMMARY: 1. How do we tie the squabble at AHS to Neolithic disease generation? 2. How does a cell react to acute stress and what results? 3. How does this stress get measured by labs and my doctor? 4. What happens when this stress lasts too long? 5. Why cholesterol is always good for [...]