READERS SUMMARY: WHAT REALLY IS A CONCUSSION? HOW DO I TREAT A CONCUSSION IF IT HAPPENS? WHAT THE MILITARY,NFL, NHL,MLB, NBA and NCAA SHOULD DO NOW? WHAT EVERY PARENT NEEDS TO KNOW NOW? Today marks the fourth blog in this series. Today also marked another early death in the NFL community. This time Orlando “Zeus” Brown was found dead in Baltimore. He was a mammoth offensive tackle who played in the NFL from 1994 to 2005. After hearing about it today I decided to post this blog tonight. I think this information is critical and needs to be considered by everyone at risk right now. Concussion is a trauma-induced alteration in mental status that may or may not involve loss of consciousness. Headache, confusion and amnesia are the hallmarks of concussion. The confusional episode and amnesia may occur immediately after the blow to the head or several minutes later. I have also seen symptoms appear several days later from concussions especially in the younger patient and in the multiply concussed patient. Sources of Concussion: Blasts Vehicle crashes Projectiles Falls Sports injuries Symptoms of concussion: · Headaches or neck pain that do not go away; · Slowness in thinking, speaking, acting, […]Continue Reading
READERS SUMMARY: 1. HOW DOES CONCUSSION, MSG, AND NEURODEGENERATIVE DISEASE ALL FIT TOGETHER? 2. WHO IS AT RISK? DOES AGE MATTER? DO I KNOW ANYONE WHO HAS HAD THIS? 3. IS ANCEL KEYS A PLAYER IN THE MSG NIGHTMARE TOO? 4. HOW IS ALS TIED TO CONCUSSIONS AND TO EXOGENOUS and ENDOGENOUS EXCITOTOXINS? 5. ARE CONCUSSIONS, AD, ALS and MSG BASICALLY THE SAME DISEASE? In the first two blogs (1) (2) in this series we looked at the fundamental neurobiology of how excitatory neurotransmitters and exogenous food additives can cause human disease. We discussed that the mechanism of disease progression is affected by age, species, and the energy status of the neuron at the time of exposure or injury. Today we are going to explore how acute neurologic aspects of cranial trauma relates to progression to long term neurodegenerative disease. We also must remember that these athletes, soldiers, and high school students are simultaneously ingesting huge amounts of MSG and aspartate in a standard American diet. I would hope that every person reading this would avoid exogenous sources of excitotoxins going forward. This is especially true if you have sustained a traumatic brain injury or a concussion in your lifetime. […]Continue Reading
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 2 of this series, we will explore how excitatory amino acids in foods and introduced to our GI tract could cause us some problems with normal functioning causing weight plateaus. We will discuss how MSG and aspartame (Nutrasweet), could wreak havoc with the human brain. This is especially true if that brain already has been concussed many times or is afflicted with some neurodegenerative disorder or is connected to an already leaky gut (low HDL level). Many people don’t seem to understand how MSG and artificial sweeteners cause damage to neurons. The experimental data on this area is documented quite well by Dr. John Olney. His work began in 1969. He studied the endocrine effects of MSG on the hypothalamus. Most of my blog readers know that leptin signaling in the hypothalamus is critical for developing obesity and controlling weight among other things. You might […]Continue Reading
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, aspartate, and glycine tie into this story? This series of blogs is going to focus in on neuronal injuries and how they all have a common tie to defective energy metabolism. The initial blog will be heavy on biochemistry but it will set the tone for you gaining a deeper appreciation of how damage to a receptor in our brains may cause different diseases, but have very common symptoms. I have focused in on energy depletion in some neurodegenerative diseases already, but we need to expand the net to explain how cerebral concussions and dietary choices are linked and can cause a less than optimal result for the person suffering from it. In this series I will also write a blog about chronic traumatic encephalopathy (CTE) since football season is now in session and this injury tends to make news in the fall sports sections. […]Continue Reading
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.Continue Reading
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% of cases.Continue Reading