Melanotan-II is a unique peptide that exerts profound effects on melanogenesis, which is a fancy way of saying “It makes you tan”. Many online users experience rapid tanning, increased sexual arousal and fat loss. But are there concerns about its use? Read on to learn more about this fascinating research compound, and hear how one user discovered that overdosing can lead to serious health concerns.

Melanotan-II was developed at the University of Arizona in an attempt to find a synthetic analog of our own body’s tanning hormone, Alpha-Melanocyte Stimulating Hormone, or a-MSH. Researchers were hoping to discover a way to protect the skin from radiation damage which leads to melanoma, aka skin cancer. When Melanin is stimulated, not only does the skin get darker, but it is also protected from the effects of excessive Ultraviolet Radiation exposure. The naturally occuring a-MSH worked well,  but it had a catch. Once injected, it did not last but a few minutes before it was a broken down in the body and rendered useless. So scientists set about figuring out how to make an analog that would last much longer. After testing hundreds of variations, they finally came upon two very effective agents, which have been named Melanotan-1 and Melanotan-2 (I will use the roman capital II as a two in some instances, but it is interchangeable, really).

Human trials then began and one interesting side effect seemed to “come up” quite often in men. Melanotan was found to increase penile erections, sometimes spontaneously so. One study concluded that a dosage of .025mg per kg every other day was all that was needed to produce this desired side effect, without any other excessive side effects. For a 200 pound man, this dosage would be 2.25mg. FWIW, I think this dosage is much higher than necessary, and in fact would cause a side effect that I find very unpleasant. It causes a very distinct and acute bout of nausea. After repeated exposure this side effect tends to weaken, but nonetheless it is still noticable to a certain degree. Most users report that no more than .25 – .5 mg is needed to achieve a darkening of the skin and increased arousal.

There is also another side effect worth mentioning. Some users who have a lot of freckles and don’t spend a decent amount of time in the sun while using Melanotan, experience a darkening of all freckles. In quite a few instances, people find that tiny, almost unnoticeable freckles become dramatically darker which makes it appear that new freckles have been formed. This side effect tends to go away once the user has stopped using the Melanotan. Once a good tan has set in, the freckles become less and less noticable.

Another pleasant side effect of Melanotan is increased lipolysis.

In addition, central application of the MC3/4-R agonist melanotan-II decreases body fat (increases lipolysis) beyond that accounted for by its ability to decrease food intake.

Some users report that taking melanotan during periods of fasting tends to yield positive recomposition benefits.

Melanotan has been available as a research peptide for many many years now. It is in no way considered acceptable for human consumption and has never been approved for a legitimate use, beyond scientific testing. Most of what I am discussing here has been old news for quite some time. But what I stumbled upon the other day made me stop and take notice.

What I found here was a case of an overdose which lead to some serious health complications.

A 39 year old male injected 6mg of Melanotan II. Two hours later, he stumbled into an emergency room and was complaining of body aches, sweating and anxiety. This blood pressure was high and his heart rate was at 130bpm, both very serious indicators of an overdose. After further investigation, the medical staff concluded that the patient was also suffering from rhabdomyolysis, which is the rapid breakdown of muscle tissue, which leads to kidney problems. The patient eventually recovered, but this makes a strong case for considering the respect users most show for products like this. I have talked about rhabdomyolysis on a few separate occasions and while excessive overtraining can cause this problem, so can the use of certain drugs, especially if taken at excessive dosages.

I tend to go through supplement kicks and phases like most other supplement hoarders I know of. When the dust settles though, there are usually a few supps that remain in my arsenal over the years. They usually stick around because they are beneficial enough for me to notice when I’m NOT taking them, as opposed to the initial buzz I notice from adding some gimmicky pill to my regimen. Chromium has gone in and out of my supply quite a few times. Recently I have been focused on reducing inflammation. While some of the basics like Curcumin, Milk Thistle and NAC come to mind, I also know that Insulin causes a great deal of inflammation chronically, and anything done to quiet Insulin will also help to quell inflammation. So I dug up an old bottle of my Chromium and started taking it again. Here’s what followed.

The next day I felt noticeably better, more energetic, less groggy and achy. Not like I was reborn or anything, but I am sensitive to subtle changes in my chemistry and biology and something was definitely different. I continued taking Chromium until I ran out, at about 200mcg per day. After a few days of being out of it, I started feeling sluggish. I picked up a bottle of Cinnamon extract with Chromium @ 400mcg per dose and then did some digging to see if I could learn anything else about this trace mineral. What I found was more than I bargained for. I knew it was good for maintaining Insulin sensitivity, but what I didn’t know is that it also had some fairly powerful effects on neurotransmitters.

From here

Chromium treatment decreases the sensitivity of 5-HT2A receptors.
Attenburrow MJ, Odontiadis J, Murray BJ, Cowen PJ, Franklin M.
Source

University Department of Psychiatry, Neurosciences Building, Warneford Hospital, Oxford OX3 7JX, UK.
Abstract
RATIONALE:

Recent case series suggest that chromium picolinate in doses of 400 microg daily may have antidepressant properties, perhaps through increasing the peripheral availability of tryptophan for brain serotonin (5-HT) synthesis.
OBJECTIVES:

To determine the effects of chromium treatment on plasma tryptophan availability and on brain 5-HT function in human and animal models.
METHODS:

We studied the effects of short-term chromium supplementation on plasma concentrations of tryptophan and other large neutral amino acids. Brain 5-HT function was assessed by measuring the corticosterone/cortisol response to the 5-HT precursor, 5-hydroxytryptophan (5-HTP), a response believed to be mediated via indirect activation of 5-HT(2A) receptors.
RESULTS:

In rats, chromium increased peripheral and central tryptophan availability and elevated brain 5-HT content. Changes in peripheral tryptophan availability were not seen in humans but in both rats and humans, chromium lowered the cortisol response to challenge with 5-HTP.
CONCLUSIONS:

Chromium can modify brain 5-HT function in humans and animals, perhaps by altering the sensitivity of central 5-HT(2A) receptors.

So from the study we see that normally 5htp ingestion, which is a popular over-the-counter serotonin precursor, will increase cortisol output. It is believed that it does so by making Serotonin that eventually agonizes the 5ht2a receptor. With Chromium, however, the sensitivity of that 5ht2a receptor is modified which alleviates that cortisol increase from 5htp supplementation.

It might seem surprising at first, but when you learn that Chromium shows promise in treating Atypical depression, it becomes clear that there is something more to this than just decreasing insulin. At the same time, we also understand that inflammation precedes most modern illness, whether it is the cause or it is an effect remains to be argued for each specific case. Depression is no exception.

First, a little bit about Atypical depression. Contrary to what the name seems to suggest, Atypical depression is actually a pretty common form of depression. Most people who are depressed but are not hospitalized for it, fall under the blanket of Atypical depression, which includes symptoms such as increased appetite, sleepiness, sluggishness and sensitivity to both rejection as well as positive reinforcement (known as mood reactivity). That last part simply infers that most people who are not depressed will usually not overreact negatively to bad news, nor will they overreact to something good happening. They are even-keeled. Someone with Atypical depression will feel a very strong sting of pain when rejected and will actually exhibit similar stress symptoms when something good happens, even though the label they will give it may sound “good” rather than “bad”. It’s the reactivity we are looking at here.

To understand a little more about Atypical Depression and how Chromium may benefit those with Atypical Depression, read this link.

Just a few key points.

Patients who were diagnosed with Atypical depression were given a placebo or a 600mcg dose of Chromium. 54% of those in the Chromium group had an improvement in symptoms whereas the placebo group only had a 34% rate of success. As an aside, it never ceases to amaze me how much placebo affects a person’s mood.  Nevertheless, the positive response in the Chromium group was nearly double the placebo, so this is noteworthy.

Most of the research done with Chromium and depression falls under the “get your blood sugar sorted out and everything else falls into place” camp. While I am in complete agreement with that statement, there seemed to be something more at work here when I was starting up my use of Chromium. There was a definite mood shift. It wasn’t good or bad per se, but something felt different. The aforementioned article on Chromium and 5ht2a receptors seems like I might be on to something.

There may also be something about Chromium that affects Norepinephrine, according to this pdf, but again anything that affects 5ht2a will also indirectly affect Serotonin and Norepinephrine release in the brain stem.

I wrote an article recently about Melatonin and promised a follow up article on how to use it, if at all. I’ve been really distracted lately and I want to do that article the justice it deserves, so in the meantime I thought I’d share a little finding I made a month or so ago about an unusual combination of Buspar and Melatonin. The results are incredibly interesting.

Buspar (buspirone) is a very old anti-anxiety drug that is truly hit or miss. For a lot of people, it does very little, if anything at all, to decrease anxiety. For some people, however, it is a godsend that rivals sliced bread. I think a lot of people find it to be less than satisfactory because they previously used Benzodiazepines such as Clonazepam or Alprazolam or even Etizolam to treat their anxiety. These are GABA related drugs and have a profoundly different impact on anxiety. They are immediate, effective and unfortunately come with a nasty reputation of withdrawal and tolerance issues. For those that have used benzos in the past, the seemingly weak and slower acting Buspar fails to meet their expectations or treat their disease.

A little bit of background info on Buspar, because I find it fascinating.

Buspirone is a partial agonist at the 5ht1a receptor, and this is believed to be the main reason why Buspar is effective for treating anxiety. Another effect of Buspar is the antagonism, particularly at the presynaptic receptors of Dopamine (D2 to be more specific, but D3 and D4 are also affected, although somewhat less so). This actually causes an increase of dopamine release. When a presynaptic receptor is antagonized, the body senses that levels of that specific neurotransmitter must be low, so it releases more, post-synaptically. Buspar is also a weak A1 adrenoreceptor agonist. This is a case similar to the antagonism of D2, in that agonizing the A1 receptor leads the body to believe that there is too much adrenaline being released, so adrenalin levels are lowered.

Buspar has been used in the treatment of cocaine dependence, alcohol withdrawal and traumatic brain injuries with enough success to warrant further research. Buspar can take several weeks to have a positive effect on anxiety, and yet for some people, there is a slight acute reaction that can either alleviate or aggravate anxiety, depending on the patient.

Melatonin has been beaten to death. If you read my previous article on Melatonin, you’ve probably learned that it can be useful, but it can also be disruptive to the circadian rhythms if used improperly (at excessive doses or timed inappropriately), but is also a very powerful anti-oxidant. I would wager to guess that most people living in an industrialized nation have a pretty pronounced disruption of their circadian rhythms and melatonin release. Darkness signals the pineal glad to release Melatonin and most of us are exposed to way too much light way too late in the evening. Even during the night, a few weak sources of light, such as alarm clocks and power buttons on appliances can produce enough light to disrupt the rhythm of Melatonin release. A good practice for those wishing to optimized their Melatonin release is to restrict light after 9 oclock, and wear a sleeping mask at bedtime. It is also crucial for the sleep patterns to be normalized, retiring at the same time every night and waking up with similar consistency.

Melatonin has been studied for its use in alleviating depression for a long time. Several attempts at creating an anti-depressant that agonizes the Melatonin receptor have shown promise, although not completely successful. A notable example is Agomelatine, but even this chemical has other effects at serotonin receptors that may explain the limited anti-depressant effect, so it’s almost inconsequential to the discussion.

So what happens when we combine the two?

The results of a study were published in December of 2012, which shows the combination of Buspar and Melatonin at night can lead to alleviation of Major Depressive Disorder. Unlike SSRI’s, which have become a gold standard in the treatment of depression, The combination of these two odd-ball compounds is not dependent upon manipulation of serotonin or any other major neurotransmitter.

Instead, the researchers believe the positive benefit lies in the increase of neurogenesis that follows administration of these two compounds. By the way, if you’re wondering what the dosages were, the study used 15mg of instant release Buspar (briggs-meyer received a patent for a time-released version but never actually produced it, which would have been quite promising because Buspar has a ridiculously short half-life and a time released version may have shown some seriously beneficial differences compared to its instant-release parent drug) and 3 mg of Sustained release Melatonin.

SSRI’s along with other anti-depressants such as tricyclic anti-depressants, all seem to increase neurogenesis, particularly in the hippocampus, which is responsible for the formation of memories. What does this mean in simple terms? I think the best way to describe the phenomenon is this: Stressful events, along with an inclination to inadequately respond to stressful events can lead to the loss of neurons in the hippocampus. Positive thinking and health moods are actually produced by certain neural pathways. In other words, we have “learned” how to be happy. We have the ability to make choices about how we feel and respond to situations. In a healthy brain, that network of connections is alive and well, and when a stressful event occurs, it is easy to find a way to think about it that produces a positive response to that stressor. With depression, those networks begin to unravel, and begin to deteriorate, leaving just a few pathways left. Those neurons tend to produce negative thinking. Again, another way to think of it is that we slowly lose the ability to do anything but the one or two behaviors or attitudes that have survived this burn-off process. When the brain’s ability to make new connections is restored through the use of drugs such as Buspar and Melatonin, new choices for behaving and thinking begin to emerge and we slowly find ourselves out-thinking the depressive thoughts and behaviors that became second nature to us.

So while there are several different types of anti-depressants, and each one of those options tend to work slightly differently (in the case of tianeptine, it actually increases the storage of serotonin, so it lowers serotonin levels available in the synapse) but in the end achieve the same result, an increase of options, of new behaviors and attitudes that will allow us to cope with the stress and think about things in a way that promotes happiness and relief.

So how exactly does Buspar and Melatonin do this? Researchers are just beginning to look at this. It has been shown in this study, that neither drug on its own was capable of producing the same resulting increase in growth, so there is something uniquely magical about the combination of these two agents which deserves further examination.

The irony of this is that I had recently acquired a decent amount of buspar, and I had recently begun taking melatonin again to try and help with sleep. I decided, after reading this article, to give the combination a go,  and I’m not really sure how I feel about the results. I have tried three or four times now to take the combination, and each time I wake up in the morning with a feeling of unease. I am not sure if it is placebo, or if it is an acute reaction that will fade with time. I am certain of one thing though: I will be trying this combination again starting tonight and will stick it out for at least two weeks before making my decision as to whether or not it will be a useful tool for my own personal growth and emotional well-being.

If any of you have had the opportunity to try these two medications in tandem, I would love to hear your results, positive or negative!

The Combination of Buspar and Melatonin in Treating Major Depressive Disorder

We used in vitro neurogenesis-based human neural stem cell (hNSCs) assays and rodent in vivo behavioral assays to identify potential novel antidepressants. A combination of buspirone and melatonin displayed antidepressant activity in these assays whereas neither buspirone nor melatonin alone showed any antidepressant-like profile. After evaluating numerous combination ratios, we determined that low dose buspirone 15 mg combined with melatonin-SR 3 mg yielded optimal antidepressant efficacy in our pre-clinical platform. The low dose of buspirone suggested that antidepressant efficacy might be achieved with only minimal adverse event liability. Based on these data, we conducted an exploratory 6-week, multi-center, double-blind, randomized, placebo- and comparator-controlled study of the combination of buspirone and melatonin in subjects with acute Major Depressive Disorder (MDD). The combination treatment revealed a significant antidepressant response in subjects with MDD on several measures (Clinical Global Impression of Severity and Improvement, Inventory of Depressive Symptomatology) compared to either placebo or buspirone 15 mg monotherapy. These preliminary findings have clinical implications and suggest that a platform of pre-clinical neurogenesis matched with confirmatory behavioral assays may be useful as a drug discovery strategy.

For a while now I have been harping on excess carbohydrate being a huge problem for those of us trying get or stay lean. It’s not so much that carbs are an enemy that must be completely eliminated, although some would argue with me on that, but it’s more so limiting carbohydrate during periods of intentional fat loss will be incredibly advantageous. I have also discussed inflammation and on a few occasions I talked about Gluten, the problems it can cause, and one possible way to treat the problem should you be a gluten for punishment, oh man that was too easy. But now, there’s something really exciting surfacing in the research that shows us a Gluten Free diet might not only make you feel better, but will also help shed excess fat.

First a quick primer on Gluten. Gluten is a protein found in wheat. It is what makes bread have the wonderful, chewy texture it has, and helps the yeast that makes it rise. The word itself, comes from the Latin word for Glue. As some of you who are already Gluten Free know, take the Gluten out of certain things like bread and you have some lame bread, even if it is made with flour of another ilk. There are some decent substitutes that you can toast and then dump peanut butter on it in order to hide it, but the truth remains, Gluten is what made bread good.

Gluten is composed of Gliadin and Glutenin are the two components that make up Gluten, which is what gives bread its protein content. Yeah, that’s right, if you’re counting the protein from your bread, please know that this type of protein may be causing you more harm than good.

So why is Gluten bad for you? Well firstly, there are some people who will say this is just a fad and that Gluten is only a problem for those with Celiac Disease. Those with Celiac would be devastated by the effects of consuming Gluten because they lack the ability to digest Gluten, which leads to severe gastrointestinal issues.

But the truth is, many of us who are not Celiac still experience a certain degree of gluten intolerance, meaning we can’t fully break it down. Why is that a problem? Well the main reason is that our immune system thinks Gluten is a foreign invader that needs to be attacked. That sets off a chain reaction of inflammation which leads to a host of other problems. Sometimes that gluten stays trapped in our intestines, where the inflammation is limited to our intestinal wall, which in and of itself is a bad thing anyways, especially considering the largest part of our immune system lives in our gut. But what happens with Gluten is even trickier than that.

Essentially, Gluten can, in some people, cause a Leaky Gut. What does that mean? Well let me explain it like this. Do you remember the last time you had a severe stomach flu and experienced diarrhea? Where did all that water come from? Well, there is a way for the intestines to open up, allowing the water in your body to fill the instestines and help evacuate it, so that the parasite can be flushed out. I know, that’s not pretty but bare with me.

Gluten possesses the same ability, in that it can tell the intestinal wall to open, and then it can enter the blood stream undigested. Then it floats throughout the whole body, getting attacked by our immune system. Ultimately, we pay the price for our immune system trying to eradicate this foreign object. We pay the price through symptoms like

• Gastrointestinal problems which may include bloating, pain, gas, constipation, and diarreah
• Aching Joints
• Depression
• Eczema
• Headaches
• Fatigue
• Infertility, irregular menstrual cycle, and miscarriage
• Cramps, tingling and numbness

Why does it do this? Essentially, according to some scientists, Gluten is a protective mechanism designed to keep the wheat seeds from being eaten. After all, that seed is destined to fall to the earth and plant a new wheat plant. You see, plants don’t want to die, or more accurately, plants do not want you to threaten their ability to reproduce.

Wheat seems to get the worst rap of all, but pretty much all cereal grains contain “prolamines” that are designed to do exactly the same thing as Gluten. Gluten however, seems to be the most offensive of them all.

Here is a great article, written in plain language, that will help you understand exactly what is going on when we eat Gluten. Again, we all experience a good part of this “infiltration” of Gliadin, but Celiac disease sufferers have a major auto-immune response to it which can be crippling. Healthy people will just feel like shit.

Don’t believe me? I understand, and I think it’s perfectly natural to be skeptical. After all, the buzzword today is Gluten Free and yet modern nutritional science doesn’t want to admit that wheat, or any other cereal grain is harmful to anyone other than celiac or allergy sufferers. But the truth is in the experience.

If you don’t believe what I am saying, then I beg you to cut out gluten for a week. Just one week – 7 days. I’d even try to get you to go grain free for a week, but let’s not push ourselves over the wall. Just cut out Wheat. So you can have oats, rice, potatoes, sweet potatoes, bananas, and corn as your starch sources. That’s plenty to choose from. Go just one week without Gluten and then on the 8th day, eat a ton of gluten. Go out to the store, buy a loaf of wheat bread and just go to town on it, eat five or six pieces. In about 20 minutes you will begin to feel what it feels like to eat Gluten. Try it, let me know how it works out for you. I’m dead serious.

Now, onto the whole point of this article. I know that Gluten is bad for me, although I will be the first to admit that I do eat it from time to time, but I always can tell when I’ve had too much of it now that I did the test I explained in the paragraph above.

What prompted me to write this article, rather than the follow up to the Melatonin Article I promised (don’t worry, I’m going to get to it!) is that the results of this study were astounding. AND, to boot, it was done on ANIMALS! Why does that thrill me so much? Because I believe animals have been eating grains for a lot longer than humans have. Animals will eat anything that grows and have existed for even longer than modern day humans have. So these animals that have evolved to eat foods like this still end up benefiting from removing gluten from their diet. Or, perhaps most animals have learned over the years not to bother with wheat because it made them feel like crap? Whatever the case may be, the following study really opened my eyes.

Gluten-free diet reduces adiposity, inflammation and insulin resistance associated with the induction of PPAR-alpha and PPAR-gamma expression.

Gluten exclusion (protein complex present in many cereals) has been proposed as an option for the prevention of diseases other than coeliac disease. However, the effects of gluten-free diets on obesity and its mechanisms of action have not been studied. Thus, our objective was to assess whether gluten exclusion can prevent adipose tissue expansion and its consequences. C57BL/6 mice were fed a high-fat diet containing 4.5% gluten (Control) or no gluten (GF). Body weight and adiposity gains, leukocyte rolling and adhesion, macrophage infiltration and cytokine production in adipose tissue were assessed. Blood lipid profiles, glycaemia, insulin resistance and adipokines were measured. Expression of the PPAR-α and γ, lipoprotein lipase (LPL), hormone sensitive lipase (HSL), carnitine palmitoyl acyltransferase-1 (CPT-1), insulin receptor, GLUT-4 and adipokines were assessed in epidydimal fat. Gluten-free animals showed a reduction in body weight gain and adiposity, without changes in food intake or lipid excretion. These results were associated with up-regulation of PPAR-α, LPL, HSL and CPT-1, which are related to lipolysis and fatty acid oxidation. There was an improvement in glucose homeostasis and pro-inflammatory profile-related overexpression of PPAR-γ. Moreover, intravital microscopy showed a lower number of adhered cells in the adipose tissue microvasculature. The overexpression of PPAR-γ is related to the increase of adiponectin and GLUT-4. Our data support the beneficial effects of gluten-free diets in reducing adiposity gain, inflammation and insulin resistance. The data suggests that diet gluten exclusion should be tested as a new dietary approach to prevent the development of obesity and metabolic disorders.

So it looks as if a Gluten Free diet not only keeps you free of the miserable inflammation that is caused by Gliadin, it also unleashes your body’s own fat burning machinery. PPAR-alpha has been talked about a lot here. It is a mitochondrial enhancer which turns the liver into a fat burning machine. Fish Oil, Sesamin and certain cholesterol lowering drugs are all PPAR-alpha activators. LPL is Lipoprotein Lipase is an enzyme necessary for healthy cholesterol metabolism. HSL, hormone sensitive Lipase is an enzyme needed to release stored fat from adipose tissue (Raspberry Ketones, Norepinephrine and Capsaicin all cause a significant increase in this enzyme and this is what makes these drugs effective for fat loss). CPT-1, Carnitine palmitoyl transferase is an enzyme that is essential for fatty acid metabolism. In some instances, people dieting may lack the necessary carnitine in order to keep this particular mitochondrial tool running efficiently.

So the long and short of it is that a Gluten Free diet will not only keep you feeling fantastic, give you healthier skin, cut down on bloat and water retention, but it will also help you lose fat. For those of you who are reading this and want to get started on a Gluten free diet I urge you to do this: Don’t get sucked into the Gluten Free section of the grocery store just yet. Focus on Lean meats, healthy fats, veggies, a little rice, corn or sweet potato, and then fruit for desert if you must have something sweet. The good news is, according this article, unless you have a ton of weight you need to lose, you may very well be able to keep the same caloric intake you have in the past and still experience fat loss. Give that diet 30 days and you will be sold on it for life! And trust me, if you do this long enough, you’ll soon discover that the way you used to feel – tired, worn down, achey, itchy, or just plain bloated, will be a thing of the past.

If you’ve ever needed a little help sleeping, you may have reached for a bottle of Melatonin. Little did you know, you may have a potent anabolic agent in your hands. Ok, so it’s not a steroid, and there are limitations and questions I have about this study, but I think you’ll find this one interesting.

First let’s talk a little about Melatonin and what does. If you happen to have a solid circadian rhythm, and you sleep in total darkness, then there is a little gland in your brain known as the Pineal gland, that will release a tryptamine type chemical otherwise known as N-acetyl-5-methoxytryptamine or Melatonin. Like I said previously, I have reason to suspect that many of us suffer from circadian disturbances and have excess light bleeding into our rooms at night when we sleep, and it doesn’t take a lot of light to affect, or rather disrupt Melatonin release. Even the late evening hours before you go to bed are supposed to be a time of very dim light. The Melatonin release is a slow and gradual one, and living in an artificially lit world is wreaking havoc on our Melatonin release.

Exposure to Room Light before Bedtime Suppresses Melatonin Onset and Shortens Melatonin Duration in Humans

Results:

Compared with dim light, exposure to room light before bedtime suppressed melatonin, resulting in a later melatonin onset in 99.0% of individuals and shortening melatonin duration by about 90 min. Also, exposure to room light during the usual hours of sleep suppressed melatonin by greater than 50% in most (85%) trials.

Parkinson’s disease (PD) is the second most common neurodegenerative disorder after Alzheimer’s disease. It is characterized by a progressive loss of dopamine in the substantia nigra and striatum. However, over 70% of dopaminergic neuronal death occurs before the first symptoms appear, which makes either early diagnosis or effective treatments extremely difficult. Only symptomatic therapies have been used, including levodopa (l-dopa), to restore dopamine content; however, the use of l-dopa leads to some long-term pro-oxidant damage. In addition to a few specific mutations, oxidative stress and generation of free radicals from both mitochondrial impairment and dopamine metabolism are considered to play critical roles in PD etiology. Thus, the use of antioxidants as an important co-treatment with traditional therapies for PD has been suggested. Melatonin, or N-acetyl-5-methoxy-tryptamine, an indole mainly produced in the pineal gland, has been shown to have potent endogenous antioxidant actions. Because neurodegenerative disorders are mainly caused by oxidative damage, melatonin has been tested successfully in both in vivo and in vitro models of PD. The present review provides an up-to-date account of the findings and mechanisms involved in neuroprotection of melatonin in PD.

Melatonin even enhances weight loss.

Melatonin and the Metabolic Syndrome

The overall findings suggest that melatonin should be exploited as a therapeutic tool to prevent or reverse the harmful effects of obesity and its related metabolic disorders.

It seems like most of Melatonin’s benefits come from its downstream expression of other hormones and genes, and its extremely powerful anti-oxidant status.

Melatonin as an antioxidant: biochemical mechanisms and pathophysiological implications in humans.

Numerous in vitro and in vivo studies have documented the ability of both physiological and pharmacological concentrations to melatonin to protect against free radical destruction. Furthermore, clinical tests utilizing melatonin have proven highly successful; because of the positive outcomes of these studies, melatonin’s use in disease states and processes where free radical damage is involved should be increased.

Melatonin also increases Growth Hormone, and it does so in a way that is unique from Growth Hormone Releasing Hormone.

Our data indicate that oral administration of melatonin to normal human males increases basal GH release and GH responsiveness to GHRH through the same pathways as pyridostigmine. Therefore it is likely that melatonin plays this facilitatory role at the hypothalamic level by inhibiting endogenous somatostatin release, although with a lower potency than pyridostigmine. The physiological role of melatonin in GH neuroregulation remains to be established.

And to finally get to our last, and most recent finding, Melatonin can help rapidly heal crushed muscle damage. NOW, before I post the excerpt I want to make my opinion clear on something. I am not a biologist, but everything I have learned thus far tells me that it is not entirely useful to compare blunt trauma type muscle damage with the kind of damage we do to our muscles during exercise. There are some similarities but I often wonder if this kind of trauma involves a different set of hormones, inflammation etc. It could be also argued that muscle damage is muscle damage. If anyone has something to share on this, please fire away!

Melatonin restores muscle regeneration and enhances muscle function after crush injury in rats.

These data support the hypothesis that melatonin supports muscle restoration after muscle injury, inhibits apoptosis via modulation of apoptosis-associated signaling pathways, increases the number of satellite cells, and reduces inflammation.

The two things I think are worth pointing out is that melatonin increased satellite cells and reduced inflammation, two very good things when it comes to recovery from exercise. But it should also be pointed out that these test subjects were rats AND they were given intraperitoneal administered doses of melatonin. That means it is injected directly into the body cavity (I know, it doesn’t sound pretty, at all…)

So what do we do to increase Melatonin levels? Well the easiest way would be to simply buy a bottle of it and pop it in your mouth. But what dosages are the best? Should you use Time-Release? Should you only take it at night? Will taking Melatonin disrupt your own body’s production of Melatonin?

I will be writing my next article to address these very questions shortly!

During my digging I stumbled upon some studies discussing the effects of Galanin, and a novel peptide called Galanin Like Peptide (GALP). While this peptide and it’s receptors have been studied for some time, this is my first run-in with the info I’ve been uncovering. It looks like we may have a potentially exciting and interesting avenue to control food intake and mood disorders such as anxiety and depression.

Galanin is a neuropeptide that is widely expressed in the brain, spinal chord and gut of humans. The majority of Galanin’s effects are still a mystery waiting to be unfolded, but there is quite a bit of evidence pointing to its neuroprotective abilities, its notable effect on food intake and regulation of mood disorders.

Neurochem Res. 2012 Nov 30. [Epub ahead of print]
Novel Galanin Receptor Subtype Specific Ligand in Depression Like Behavior.
Saar I, Runesson J, Järv J, Kurrikoff K, Langel U.
Source

Institute of Technology, University of Tartu, Tartu, Estonia, indrek_saar@hotmail.com.
Abstract

Neuropeptide galanin and its three receptors, galanin receptor type 1-galanin receptor type 3, are known to be involved in the regulation of numerous psychological processes, including depression. Studies have suggested that stimulation of galanin receptor type 2 (GalR2) leads to attenuation of the depression-like behavior in animals. However, due to the lack of highly selective galanin subtype specific ligands the involvement of different receptors in depression-like behavior is yet not fully known. In the present study we introduce a novel GalR2 selective agonist and demonstrate its ability to produce actions consistent with theorized GalR2 functions and analogous to that of the anti-depressant, imipramine.

In the study quoted above we can see that there are three types of Galanin receptors, type 1, 2 and 3. It also appears to be that the type 2 receptor has the most beneficial impact on alleviating depressive behavior. Unfortunately, the researchers conclude that they have not yet developed or discovered a ligand that will bind selectively to the galanin type 2 receptor in order to verify their hypothesis.

Here’s an interesting study discussing Neuropeptide Y, another major player in the control of food intake, and Galanin. What’s unique about this article is that it discusses the effects of High Altitude on food intake, an inter-relation I had no idea existed until now.

Role of neuropeptide Y and galanin in high altitude induced anorexia in rats

Anorexia causing weight loss at high altitude (HA) is a major problem. Neuropeptide Y (NPY) and galanin are considered to have appetite regulatory function. The present study was therefore undertaken to investigate the changes in these two peptides at simulated HA and its possible role in anorexia. Male Sprague-Dawley rats (n = 8 in each group) were exposed to simulated HA (7620 m) for 1, 7, 14 and 21 days for 6 h a day and to an altitude of 6,096 m for 72 h to study the effect of intermittent and continuous exposure, respectively. NPY and galanin levels were estimated in different brain parts and plasma of exposed and unexposed control animals. Significant reduction in food intake was observed in rats during both intermittent as well as continuous exposure. In case of 72 h continuous exposure severe reduction in food intake was observed (73.2%) with reduction in body mass (approximately 29.7g/rat in 48h). Hypothalamic NPY levels were decreased by 54.7, 35.0 and 15.4% in 1, 7, and 14 days, respectively, in case of intermittent exposure to HA. However in case of 72 h HA exposure no significant change in hypothalamic and circulating NPY levels were observed. Plasma galanin levels were decreased in both intermittent and 72 h continuous HA exposed rats. Hypothalamic galanin levels were also decreased in 72h exposed rats. The changes in levels of these peptides may be responsible for anorexia at HA.

Singh SN, Vats P, Shyam R, Suri S, Kumria MM, Ranganathan S, Sridharan K, Selvamurthy W. Nutr Neurosci 2001;4(4):323-31

I am just as curious at this point, how they “Simulated” high altitude. Yikes.

But sure enough, high altitude did in fact lower both Neuropeptide Y and Galanin levels dramatically. If you were getting ready for a contest and you needed to reduce your appetite dramatically, then may I suggest a career in the Airline industry? Not very practical but interesting nonetheless.

So it appears that in the 90s there was a huge push to learn more about Galanin, not only because it seemed to effect food intake, but also affected reproduction (sex drive?).

Galanin/GALP and galanin receptors: role in central control of feeding, body weight/obesity and reproduction?

Scientific and commercial pharmacological interest in the role of galanin and galanin receptors in the regulation of food intake, energy balance, and obesity has waned recently, following initial enthusiasm during the 1980-1990s. It has been replaced by efforts to understand the role of newly discovered peptide systems such as the hypocretin/orexins, melanocortins and cocaine- and amphetamine-regulated transcript (CART) and their relationship to the important hormones, leptin and insulin. Thus, while numerous studies have revealed the ability of galanin to stimulate food intake via actions at sites within the hypothalamus, and shown reliable changes in hypothalamic galanin synthesis in response to food ingestion; findings including the lack of a ‘body weight/obesity’ phenotype in galanin transgenic mouse strains and a lack of agonists/antagonists for galanin receptor subtypes have probably served to reduce enthusiasm. However, as more is learnt about the general and galanin-related neurochemistry of brain pathways involved in feeding, metabolism and body weight control, the potential importance of galanin systems is again in focus. Studies of the newly discovered galanin family peptide, ‘galanin-like peptide’ (GALP), highlight the likely role of galanin peptides and receptors in the physiological coupling of body weight, adiposity and reproductive function. GALP is produced by a discrete population of neurons within the basomedial arcuate nucleus (and median eminence) that send projections to the anterior paraventricular nucleus and that make close contacts with leutinizing hormone-releasing hormone (LHRH) neurons in basal forebrain. Furthermore, GALP neurons express leptin receptors and respond to leptin treatment by increasing their expression of GALP mRNA. Centrally administered GALP activates LHRH-immunoreactive neurons and increases plasma LH levels. These findings suggest a direct stimulatory action of endogenous GALP on gonadotropin secretion via actions within the hypothalamus/basal forebrain, with leptin actions linking this system to body adipose levels.

Gundlach AL. Galanin/GALP and galanin receptors: role in central control of feeding, body weight/obesity and reproduction? Eur J Pharmacol 2002 Apr 12;440(2-3):255-68

So it appears that Galanin increases LH, and positively modulates Leptin, which is of course a major player in food intake. It’s important to point out that both Leptin and Galanin, while being very important in food intake and reproduction, are not simply the kinds of peptides that you just increase and get a positive result. Leptin studies have been done and we see that a good majority of overweight people have very high levels of Leptin in spite of the fact that Leptin should lower food intake. To me, this points to an issue of sensitivity. At some point in time, overeating begins to decrease sensitivity to Leptin.

So how do we try and modulate this system? I’m not sure yet. There is evidence that shows herbal adaptogens have an impact on things like Neuropeptide-Y, and I think I will uncover studies showing a connection, or we will find new research emerging showing an effect. The trouble here is the specificity of it all. When you talk about these types of peptides, you are talking about a really selective and delicate system. And as we’ve seen with Leptin, it’s not always a matter of “More is Better.”

It’s been known for a long time that supplementing with Fish Oil can be a good thing for inflammation, cholesterol and weight control. I decided to do some digging around about this basic nutrient (Omega-3 fatty acids) and what makes it so special. I stumbled upon an article talking about C-Reactive Protein and a handful of different dietary supplements.

Stick around for the entire article because I have some Omega-3 I would like to get rid of at a very reduced price.

Fish Oil is high in Omega-3 fatty acids. To be specific, it contains EPA(eicosapentaenoic acid) and DHA(docosahexaenoic acid), which are essential to our diet because our bodies cannot synthesize these particular fatty acids. Why are Omega-3 fatty acids so important? They are involved in several processes including the formation of nerves, and help activate the fat burning process in our livers due to their ability to stimulate the PPAR-alpha receptor. In addition to these effects, Omega-3s are an important family of fatty acids that help balance the other omega fatty acids, Omega-6 and Omega-9. The typical western diet is usually very out of balance in this regard, notably Omega-6 fatty acids tend to be off the charts, while Omega-3s don’t seem to be consumed much at all. The only really good source of these fatty acids is found in fish, and the second best source is found in Flax seed and a few other vegetarian sources.

C-Reactive protein is a marker for inflammation. In other words, when inflammation is sensed due to release of certain factors by macrophages or adip0se (fat) tissue, C-Reactive Protein is released by the liver where it binds to phosphocholine which is expressed on the surface of a dying or dead cell. So essentially what I’d like for you to take away from this is that C-Reactive Protein is not an inflammation causing substance. It is a messenger, a marker released by the body when inflammation has occurred. So in essence we want to reduce C-Reactive Protein, not because it causes inflammation, but because we want to effectively limit the inflammation that is signalling the release of C-Reactive Protein. To put it another way; If we reduce inflammation, we will know we have done so because levels of C-Reactive Protein will go down.

In a recent study evaluating quite a few different dietary supplements and their effects on inflammation (measured by levels of, you guessed it, C-Reactive Protein), we clearly have a few big winners and we also have a handful of duds. Interestingly enough, Glucosamine and Chondroitin were very effective at reducing C-Reactive Protein, and Fish oil followed shortly behind. If you read my article about Glucosamine and prevention of inflammation induced by gluten and lectins, you will see here further evidence that Glucosamine might just be a very effective supplement at reducing inflammation in general.

So Glucosamine, Chondroitin and Fish Oil were the stars here, all three having a strong impact on CRP. Methylsulfonylmethane(aka MSM), garlic, ginkgo biloba, saw palmetto, and pycnogenol all failed to deliver a significant decrease in CRP. That’s not to say those particular supplements wouldn’t be useful for other purposes, it’s just that they don’t seem to shine quite like the three big guns in the war on inflammation.

Incidentally, I have a whole box of Supranatural RX Omega-3 Active that I would like to sell. I originally bought a few boxes thinking I would be tearing through it at a fast clip. It turns out that I am getting exactly what I need at some lower dosages due to the highly concentrated EPA and DHA content of this product. This truly is a very solid fish oil product that I highly recommend. Feel free to order directly from them, but if you’d like to get a hold of a deeply discounted bottle,  just click on the link below to pick up 120 softgels for just 19.95 plus 7.95 for shipping.

Association Between Use of Specialty Dietary Supplements and C-Reactive Protein Concentrations.

Laboratory evidence suggests that certain specialty dietary supplements have antiinflammatory properties, though evidence in humans remains limited. Data on a nationally representative sample of 9,947 adults from the 1999-2004 cycles of the National Health and Nutrition Examination Survey were used to assess the associations between specialty supplement use and inflammation, as measured by serum high-sensitivity C-reactive protein (hs-CRP) concentration. Using survey-weighted multivariate linear regression, significant reductions in hs-CRP concentrations were associated with regular use of glucosamine (17%, 95% confidence interval (CI): 7, 26), chondroitin (22%, 95% CI: 8, 33), and fish oil (16%, 95% CI: 0.3, 29). No associations were observed between hs-CRP concentration and regular use of supplements containing methylsulfonylmethane, garlic, ginkgo biloba, saw palmetto, or pycnogenol. These results suggest that glucosamine and chondroitin supplements are associated with reduced inflammation in humans and provide further evidence to support an inverse association between use of fish oil supplements and inflammation. It is important to further investigate the potential antiinflammatory role of these supplements, as there is a need to identify safe and effective ways to reduce inflammation and the burden of inflammation-related diseases such as cancer and cardiovascular disease.

In the fall of 1924, a professor at the University of Michigan convinced the salt manufacturers of the United States to adopt the practice of adding Iodine to table salt. Iodine is an essential mineral that isn’t very abundant in our food supply. Iodine deficiency can cause serious developmental disorders, including retardation, but more to the point of this post, it can also lead to hypothyroidism. Without Iodine, the body cannot create the Thyroid Hormones, Thyroxine (T4) and Triiodothyronine (T3). Fast forward to the present time: Many people are working feverishly to reduce their sodium intake, and a lot of people have switched to “healthier” sea salts to flavor their food. The net result is that our iodine intake is slowly dropping as well. The good news is, you don’t have to choke down a spoonful of table salt to get your Iodine, the even better news is: You can keep your Thyroid kicking ass for FREE.

Before I go a little bit more into detail about Potassium Iodide, let me just spill the beans. I recently started doing some work for a supplement company that offers several solid products, ranging from IP-6 to Green Coffee bean, to Raspberry Ketones. Their newest product, called Doomsday Capsules, contains Potassium Iodide, and I’ve been given the opportunity to pass along to my readers a chance to pick up a bottle of this for Absolutely FREE. You don’t pay a dime, they’ll even front the shipping costs. I’ll go more into detail about how to get your own bottle to try out, after I make a few key points and offer a very strong cautionary comment.

The product is called Doomsday Capsules for a reason. In the event of exposure to radioactive material, god forbid, such as a nuclear plant meltdown, or a nuclear bomb explosion, having an iodide product on hand will be essential to survival. What happens is that fallout creates radioactive iodine ions that displace normal iodine in the thyroid and trash the gland until it’s completely spent. By consuming Potassium Iodide, you effectively block the radioactive iodine from getting into your thyroid. It’s very well documented and researched and has been recommended by the CDC, should you ever be exposed to something as aweful as this.

Do I expect any of my readers to ever face such a cataclysmic experience? I should hope not. So is there any use for this stuff besides Apocalypse insurance? Absolutely. If you tend to restrict your sodium intake, or you have replaced most of your table salt with sea salt, then you could be slowly depleting your iodine reserves. This will inevitably lead to sluggish Thyroid, and reduced metabolic rate. Even if you’re consuming a lot of food-stuffs (which I hope you aren’t) that sodium does not contain iodine, so again, you’re missing out on this vital nutrient.

Hypothyroidism can be a very real and dangerous situation. It can most definitely have a very negative impact on both your waistline and your general well-being. But, I’m not suggesting you run to your doctor’s office at the first sign of feeling kinda tired and scream hypothyroid! What I am suggesting however, is that before you become fully hypo, there are times where supplementing with a little bit of iodine can make a real difference in your metabolic output.

A word of Caution: Iodine is essential to your body’s health. But consuming more than the recommended amount can lead to poisoning. If you’re using the product at the full dosing, the label clearly states you should limit it to no more than 10 days. I would take it one step further. I only take one capsule a day for a few days and then reassess. I then rinse and repeat occasionally. If I’m beginning to feel a bit burned out, I can tell when my iodine intake has been low and taking a dose for a few days seems to pull me out of it. My final point on this. Please limit your usage of this. I’m not going to tell you how to take it, because I am not a doctor. Instead I can only point out what I do and hope that you would adopt an equally conservative dosing schedule.

HOW TO GET YOUR FREE BOTTLE OF POTASSIUM IODIDE

So with that covered, let me tell you a little more about the deal here. I was approached by the makers of Doomsday Capsules and I have been given the opportunity to offer a free bottle to my readers. All you have to do is email gary@geneticsolutionsllc.com and include in the message title “Metabolic Alchemy FREE Doomsday Caps”. I am even coding the link here to automatically insert that into the message title. If there is a big enough response, I’ll be working to get more deals from this company in the future on other products that I think could be really useful. Stay tuned, and Keep me updated!

In a previous post about Berberine and Skullcap I briefly mentioned that these two supplements have the ability to inhibit prolyl endopeptidase(PEP). This enzyme is responsible for breaking down peptides in the brain, and there is a strong link between mental illness and an overactive PEP enzyme system. If you decrease this enzyme you will effectively increase the life of peptide hormones in the brain, ranging from oxytocin to luteinizing hormone.

Leuteinizing Hormone (LH) is released from the pituitary gland and directs the testes to increase Testosterone production. It’s absolutely essential for the health of both men and women(it is an integral hormone in the menstrual cycle). If you happen to have an overactive PEP then you could be prematurely reducing your LH signal, and this will ultimately lead to less than optimal hormones.

I am not sure exactly how one would even go about testing for an issue like this, but honestly, I haven’t read much of anything that says decreasing it could cause any major issues, so my pioneering mindset would say “go for it” and see if it helps. If you’re depressed, or if you are interested in manipulating your own peptide status, then I would look into Skullcap, or more specifically, Baicalin, which is the main component of Skullcap responsible for the reduction of PEP.

http://www.sciencedirect.com/science/article/pii/0304394079961615

Summary

A highly purified preparation of rabbit brain prolyl endopeptidase cleaved the decapeptide luteinizing hormone—releasing hormone (LHRH) at the Pro-Gly · NH₂ bond leading to the release within 1–3 h incubation at 37°C of des-glycinamide LHRH and glycinamide. Evidence for this site of cleavage was obtained by the detection of glycinamide or glycine end groups by a microdanyslation procedure, and by separation of the breakdown products by high performance liquid chromatography (HPLC) on a reverse phase C-18 column. Incubation led to the appearance of two new peaks as detected by HPLC one of which was collected and shown to have the composition consistent with des-glycinamide LHRH. The other peak ran in the position identical to that of authentic glycinamide. Results suggest that prolyl endopeptidase could play a role in the inactivation of LHRH in vivo.

I was stumbling around the internet today and read an article about the emerging awareness of the damaging effect of Gluten. I then went on to read an article about Potatoes, Tomatoes and Rice. In that article, the author suggested that these foods have a special lectin similar to wheat germ agglutinin, which is an additional inflammatory agent found in even sprouted grains, which takes the wind out of the sails for those looking to relieve themselves of inflammation by eliminating wheat products. In this article, the author also pointed out a concept that really sparked my interest.

Sayer Ji, the author of the website, greenmedinfo.com, suggested that people taking Glucosamine products may be helping to reduce inflammation of their own tissue due to the concurrent ingestion of Wheat and other products that contain lectins. You see, almost all cereal grains, and several other fruits and vegetables have protective agents called lectins. These lectins will break down the cell walls of bacteria and other organisms that might try to consume or destroy the plant. The cell walls of these foreign invaders is made primarily out of N-Acetyl Glucosamine. Lectins break down these walls, killing the intruders, thus ensuring the survival of the plant.

Unfortunately, N-Acetyl Glucosamine is the protective coating on our joints, bones, arterial walls, etc. So in essence, wheat and other grains, and a few other legumes etc, are trying to protect themselves, and in the process, when we consume them, we are exposing ourselves to these “thorns” that bind to our tissue and cause an inflammatory reaction.

At least, this is the theory, backed up by more research than I care to dig through, that the author promotes. One of his observations about our consumption of Glucosamine products really caught my attention:

One way to gauge just how pervasive the adverse effects of these foods are among Western populations is the popularity of the dietary supplement glucosamine. In the USA, a quarter billion dollars’ worth of glucosamine is sold annually.The main source of glucosamine on the market is from the N-Acetylglucosamine rich chitin exoskelotons of crustaceans, like shrimp and crab. Glucosamine is used for reducing pain and inflammation. We do not have a dietary deficiency of the pulverized shells of dead sea critters, just as our use of NSAIDs is not caused by a deficiency of these synthetic chemicals in our diet. When we consume glucosamine supplements, the chitin-binding lectins in our foods, instead of binding to our tissues, bind to the pulverized chitin in the glucosamine supplements, sparing us from their full impact. Many millions of Americans who have greatly reduced their pain and suffering by ingesting glucosamine and NSAIDs may be better served by removing chitin-binding lectin containing foods (the underlying cause of their malaise) from their diets. This would result in even greater relief from pain and inflammation along with far less dependency on palliative supplements and medicines alike. ~ Opening Pandora’s Bread Box

So if you didn’t quite catch that, let me reiterate it. The reason why Glucosamine supplementation might be so helpful to those who are suffering from joint inflammation might not be directly related to any kind of replacement of joint Glucosamine, but may in fact be an indirect reduction of lectins in our diet, because those lectins will bind to the supplemented glucosamine rather than our joints and other tissues. He also goes on to suggest that we could probably stop taking Glucosamine all together if we just stopped eating the foods that contain these pesky lectins.

What’s interesting to me is that I always wrote off Glucosamine as junk. The science never really appealed to me, and there was always something lacking in my confidence of a product that was supposed to reduce inflammation by simply replacing lost glucosamine. In other words, I always felt like taking something like Glucosamine would really not help replace the glucosamine. Just because you take a certain mineral or substance, doesn’t mean the body will actually do anything with it. The same could be said about Calcium. You could have osteoporosis and swallow calcium tablets by the handful, but that calcium won’t magically bond with your bones unless some kind of absorption process was initiated. This is why Vitamin D is so important. We always get plenty of calcium in our diet, especially if we drink or eat dairy products. The problem lies in the “construction” process, the hormonal process that actually takes the calcium from our diet and then utilizes it.

So I always wrote off Glucosamine as a placebo. But I do remember taking it and feeling some relief from inflammation. If the author is correct, then it gives me confidence to suggest people supplement with it, especially making sure to consume it whien consuming foods that contain lectins, gluten etc.

So why is this so compelling to me, and why did I feel the need to write about it in this blog? Well, because most of us are probably consuming plenty of grains and legumes and other foods that are contributing to inflammation within the body. Inflammation causes a whole set of issues that ultimately lead to Metabolic Syndrome, insulin resistance, etc.

Also, I think it’s important to point out that I also tend to feel pretty crappy when I eat grains, and while I do my best to limit their consumption, I always tend to indulge at least once daily, because let’s face it – bread is delicious.

So I will be picking up a bottle of Glucosamine and will begin to experiment with it. I suggest you do the same. First and foremost I would suggest you educate yourself on the effects of gluten and lectins on the body. I also suggest you begin eliminating those types of food from your diet (Sweet Potatos, Oats, and Corn are starch sources that don’t contain these excess toxins). But if you aren’t planning on completely eliminating the consumption of these foods, then I highly recommend you start taking a Glucosamine product whenever you are consuming these types of foods, and see how your body responds.

I also suggest you try to find the powdered version of Glucosamine, which will allow for a quicker protective effect, allowing the lectins to bind to the Glucosamine molecules as quickly as possible.

I’ll be updating this thread in a few weeks with any observations I make, or relevant study information I discover during my digging.