Researching the viability of ketogenic diets for therapeutic usage was one of the original interests that launched this blog. And while there is growing data for brain cancers and even a Cochran review for the use of ketogenic diets in epilepsy, the bipolar story has always been theoretical.
Ketogenic (very low carbohydrate and low protein) diets should work a bit like the mood stabilizer depakote in regulating unstable moods in bipolar disorder, making them an interesting option, should the research pan out. I explore the research and details in this post:
But, as I stated in that article, there were no randomized controlled trials, not even a pilot trial, and the only two case studies I had unearthed had one guy getting psychotic on Atkins induction and another one where a hospitalized bipolar woman showed no benefit (but despite reported enthusiasm and being in an inpatient unit where her food was supposedly entirely controlled, she never achieved ketosis).
But the other day PubMed emailed me a new paper with links to the following article: The ketogenic diet for type II bipolar disorder. Thanks to the good Dr. Eades I was able to see the full text without getting a librarian to request it for me.
And here we have not one, but two rather well documented cases of bipolar II disorder in women, beginning in youth with some hypomania, in one person predictable seasonal depressions in the summer and a bit of mania in the spring. Both women had bad responses (such as suicide attempts and suicidal thoughts) to antidepressant trials and one gained weight on quetiapine. They were tried on lamotrigine, an anticonvulsant and mood stabilizer, with okay results (one woman was finally able to maintain a job and be functional). One tried a ketogenic diet to help with some irritable bowel symptoms, the other just wanted to try the diet. One woman ate raw cream, grassfed beef, organic pork, free range chicken, and seafood. The other ate mostly chicken, fish, and coconut oil with 2-3 cups of vegetables a day. Both monitored their urine with ketostix or Ketone Care Test Strips most days for several months, achieving mild to moderate ketosis on most days. Both women eventually discontinued the lamotrigine and reported better symptom control with the diet than with medication.
One woman described her irritability going away and a sense of calm. Also “having my head screwed on straight–well, it’s definitely worth giving up pie.” She said her symptoms seemed better with a ketone level of 15mg/dl vs 5 mg/dl in the urine. The other woman noted that if she remained gluten-free, she felt much better, even though she had never been diagnosed with celiac disease.
Neither woman had any adverse consequences and they remained stable on the diet for 2-3 years at the time the paper was published.
The paper details how a slight acidosis achieved with a ketogenic diet results in decreased intracellular sodium accumulation, which is the mechanism by which all anticonvulsants which are also mood stabilizers appear to work. In addition, the paper details some possible pitfalls of a ketogenic diet, such as difficulty maintaining it in a world of twinkies and coca-cola, and the risk of kidney stones. The author recommends >2.5 liters a day of fluids and a potassium citrate supplement to alkinilize the urine, which is done routinely in pediatric clinics where ketogenic diets are used for seizures, but may not be be necessary in adults. There is a long-term review of the ketogenic diets in kids (though I’m not a fan of the ingredients in some of the formulas used for tube-feeding some of these kids – soybean oil, soybean oil and more soybean oil) talking about complications over 6 years. Since these kids were often very ill with many other debilitating conditions, it is hard to attribute the complications (sepsis, cardiomyopathy, lipid pneumonia) to the diet itself.
Lipids were measured in one woman from a vegetarian to an omnivorous to a ketogenic diet. As is expected her trigs dropped and her LDL and HDL went up on the ketogenic diet. Total cholesterol to HDL ratio (the best cheap test I know of relating to total LDL particle number, with a lower ratio being better) on the vegetarian diet was 4.47, 3.78 on the omnivorous diet, and 3.74 on the ketogenic diet.
All in all, the paper is a nice illustration of two motivated patients achieving remission of their bipolar symptoms (which they had dealt with for decades) with a free-living ketogenic diet (and some other supplements, though each woman took different ones, for example, probiotics and omega 3). Two anecdotes isn’t a huge amount of data, but it is intriguing, and I would say the time for a randomized controlled trial of ketogenic diets in bipolar disorder is way overdue.
(Final note as I was in a bit of a hurry when I wrote the post at first… I did want to say there is a *lot* about these case study diets that could be therapeutic. No processed food, no sugar, lots of nutrients, lots of omega 3, low in gluten or gluten-free, likely low in histamine. The tracking of the ketones and one women’s experience that the 15mg/dl ketone level felt more calming to her along with the sensible biologic mechanism makes the ketosis part plausible, but it is important to note these other possible factors).
Source: primal docs
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Thanks to research coming out of the University of Colorado Cancer Center, and published in the medical journal Cancer Letters, those suffering from colon and rectal cancers might soon be able to ditch the cancer-causing ‘medicine’ called chemotherapy, and instead utilize a simple herbal extract with better success. Grapeseed extract (GSE) has recently been proven to prohibit cancerous cell growth and to instigate cancer cell death.
The bioactive compounds in grapeseed extract are what make chemotherapy seem like an archaic form of treatment, especially considering that chemo and radiation treatments can backfire and cause cancer to come back from remission 10 times stronger than when it was first detected. These treatments kill healthy cells, but GSE compounds including curcumin and resveratrol leave healthy cells in tact while demolishing cancerous ones.
GSE is so effective that it treats stage IV cancers with astonishing success. One of the doctors involved with the study stated, “It required less than half the concentration of GSE to suppress cell growth and kill 50 percent of stage IV cells than it did to achieve similar results in the stage II cells.” They go on to explain that GSE targets multiple mutations in cells to eliminate them and stop their proliferation in the body.
Just 150 to 250 mg per day of GSE can help to prevent colon and rectal cancers while also preventing numerous other ailments.
Curcumin and Resveratrol – More Cancer Fighter
A bio-active compound in GSE and popular supplement, resveratrol has been found to help with everything from diabetes to anti-aging; from heart disease to cancer. Chinese medicine practitioners have long known that resveratrol (found in Hu Zhang or Japanese Knotwood) can even help repair cracks in arterial linings. It has been used for more than 1500 years to treat numerous medical problems and to increase longevity.
If you can’t get your hands on grapeseed extract or simply want another cancer-preventing option. look no further than curcumin supplementation. One study on curcumins (which is the compound found in the spice turmeric) from the University of Kansas’ Cancer Center and Medical Center, indicated that curcumin inhibits the growth of esophageal cancer cell lines, though how it works “is not well understood”.
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Celiac disease: Why your body thinks gluten is a nasty invasive antigen or ‘bug’.
And how – if you keep eating gluten a vicious cycle of damage will ensue.
In this post I will set the scene for future posts on dietary strategies to treat celiac disease. A number of recent studies have shown that just avoiding gluten is not enough for many, and they also need to avoid other foods in order to reduce the gluten antibodies and inflammation in the intestine.
In this post I will explain why and how gluten is a problem for those who have a specific genotype that predisposes them to celiac disease. I won’t be tackling gluten sensitivity in this post.
Celiac disease (CD) is an immune response to gluten proteins that happens in genetically vulnerable people. Gluten is found in wheat and related cereal grains e.g. wheat, rye, barley, triticale. Gluten is a protein – not a carbohydrate – even though it is found in grains.
Protein digestion: we usually break down proteins into single amino acids
Proteins are constructed with very long chains of amino acids. There are 20 standard amino acids; imagine these being 20 different coloured beads and linked like long chains– like those beads that children snap together. Every protein molecule is constructed with a particular sequence of amino acids (i.e. the beads are in a specific pattern or arrangement). These long chains are folded and coiled, and sometimes crosslink to make a specific protein.
When we eat proteins our digestive enzymes (think of these as being chemical scissors) cut the links between the amino acids (pull the beads apart). Each different amino acid requires a different enzyme to disconnect it from its neighbour.
When these are broken down into single amino acids they then go into gut cells (enterocytes) where they are either used or sent on their way out the other side of the cell around the body to other cells. Under genetic instructions the single amino acids are joined into a specific sequence to make them into any tissue, protein or enzyme etc. that the body needs at the time.
Problem: Gluten does not get properly digested into single amino acids
The problem with gluten is that is contains a large number of 2 particular amino acids – glutamine and proline (think of these as green and purple beads), (we call these types of proteins ‘prolamines’). Humans don’t have the enzymes to break proline apart from its neighbour, so instead of breaking the long string of amino acids onto singles, it stops at a peptide, a short chain. Gluten protein breaks down into a number of different peptides that cause problems. 
It’s not gluten that is the issue – it is these short strings of amino acids that we can’t digest further. In people with celiac there is a vicious circle of effects, each peptide causing a problem that increases the toxicity of other peptides. This diagram shows a number of different parts of the gluten molecule, that cause problems.
Problem: Gluten peptides pass through the gut cell barrier from one side to the other intact where we react to them as a foreign ‘invader’.
I want you to stop and imagine your gut as being a continuation of the outside of your body, basically one big long tube coiled up inside your body, and think of the cells lining your gut as a skin.(Picture source)
The ‘skin’ of your gut is very wrinkled and folded, in fact if you took the skin of your gut and spread it out it would spread to the size of a tennis court. The large pink sheet below represents the surface area of the gut (the red is lung surface area and the green your skin):
The inside of this tube is called the lumen. It contains huge numbers of bacteria, and of course a constant flow of food and fluid. The cells in your gut secrete acid (in the stomach) and enzymes (in the stomach, pancreas and small intestine) to break down food into simple units that your body can absorb. It is only when a food particle is broken down into the simplest unit (a fatty acid, glucose molecule or amino acid) that it can be transported through the enterocyte into the fluid and bloodstream on the other side. This way we keep out large things like bacteria and viruses from getting underneath the ‘skin’. If large things do get through we have a whole host of ‘fighter’ cells waiting to nab them and deactivate them or digest them so they don’t cause trouble in the body.
You see – gluten and gluten peptides are not really a problem if they stay inside the lumen, they just end up going down the toilet. But this doesn’t happen in people with celiac disease.
Gluten peptides get through in two ways; either through the cell (transcellular) or between the cells (paracellular).
How does gluten get through the gut barrier? Scientists are fairly sure they have worked this out.
First – transcellular transport: how gliadin passes through the cell undigested
In mucous membranes there is one particular antibody called secretory IgA (SIgA). This is a first line defence responsible for keeping toxins and pathogens (bad bacteria etc.) from getting to the gut cells, it is a bit like a bouncer in a nightclub blocking the entrance so undesirables can’t get past. SIgA can also take pathogens to special areas where they can be deactivated by immune cells (sub epithelial dome), like a bouncer escorting an undesirable to the police station to get locked up. SIgA increases in your gut when there is inflammation (as there is with Celiac disease), because it needs to get to work reducing whatever undesirable is causing the inflammation.
In celiac disease something happens that shouldn’t: the SIgA (the protein that should be protecting from invaders) transports the gliadin through the cell and out the other side undamaged. How does it do this? First the gliadin peptide forms a complex with SIgA, which should take it off to get processed as a ‘baddy’ but it doesn’t – there is a doorway in the gut cell than allows the SIgA and gliadin complex to get transported in one side of the cell and out the bottom. Why does this happen when it shouldn’t?
Unfortunately in people with celiac a doorway is available for the IgA to enter with its new buddy gliadin – a doorway that normally shouldn’t be. This doorway results from the person having an iron deficiency (anaemic). People with celiac are often anaemic, as their inflamed gut does not absorb iron properly. In order to try to absorb more iron the gut cells send special iron transporting units (transferrin CD71) up to the surface of the gut cell. For some reason this receptor hooks up with the ‘bouncer’ and the ‘baddy’; the SIgA-gliadin complex, (think of the ‘bouncer’ acting like a Trojan horse that protects and escorts the gliadin) and takes it from one side of the cell to the other. From the outside of the body to the inside. Sneaky! Once on the other side the SIgA releases the gliadin.
Gliadin peptides linked to SIgA, ( secretory IgA) getting taken into cell and passing out the other side via TfR, (transferrin receptor);TG2, (transglutaminase 2) takes peptides and alters them, HLA-DQ2/8 molecule picks it up and presents it to immune cells to set up ‘kill’ response. (Source)
Paracellular pathway: How gluten creates gaps between cells so it can sneak through.
A gut cell needs to be tightly glued to its neighbour in order to prevent any undigested food or pathogens getting through this barrier. Each cell binds to its neighbour with a complex of proteins called a tight junction. This acts like glue, it lets fluid through but no large molecules. The gut cells are able to release a chemical that tells the gates to open. This chemical is called zonulin, and its release is triggered by bad (pathogenic) gut bacteria – this will let the bacteria through below the surface where it can reach the ‘fighter’ (immune) cells and get them into action.
In celiac disease, gliadin proteins interact with the gut cell, (the CXCR3 receptor, which people with celiac have more of than unaffected people), and the gut cell sends out zonulin – which ‘tells’ the tight junction to loosen up, literally opening up a pathway between cells. Now that the gate is open gliadin peptides can bypass the gut cell barrier and make their way down into the area chock full of fighter cells waiting to pounce and quell an assumed infection. 
Once through the gut cell barrier, the gluten peptide gets transformed into an even nastier peptide that triggers an immune reaction
One more thing happens in people with celiac disease. Once the gliadin gets through the gut wall it comes into contact with an enzyme called transglutaminase 2 (TG2). TG2 modifies proteins i.e. changes them a little, but it only changes some proteins, gliadin just happens to look like a one of the proteins that TG2 is supposed to change. So it gets on and does the job very efficiently, and changes it into just enough so that it fits into a little pocket on antigen presenting cells.
Bear with me – this is important but a little complicated.
Whenever we have an infection an antigen presenting cell (APC) takes a section of protein (a peptide) from a broken down bacteria, holds it in a little pocket and presents it to fighter cells. The fighter cells then go off and make anti-bodies to this so they can begin the process of spreading throughout the body and killing that specific protein (the invading bacteria). Once the invaders are killed the antibodies disappear, however the dormant fighter cells ‘remember’ this protein so if it invades again it recognises it and can replicate an army of antibodies to go fight very quickly.
People with celiac disease present a bit of protein from gluten as though it is an invading pathogen
People with CD have a particular type of APC specific to their genotype, and the gliadin altered by TG2 fits in perfectly into the little presenting pocket. (The genotype is HLA-DQ2 , specifically HLA-DQ2.5 and HLA-DQ8 which about 30% of the population has. If you don’t have this genotype – you can’t pick up gluten as it doesn’t fit in the APC’s pocket) So as soon as TG2 changes the gliadin protein in a specific way, the APC picks it up (it’s like a key that fits perfectly into a lock) and shows it to the fighter cells. (CD4+ T cells) They then go to work to fight this invader and make numerous antibodies to try to kill it off. (Gliadin antibodies)  Below is a diagram of the APC with the gliadin showing it to a T-cell.
People with CD also make anti-bodies against the important transglutaminase enzyme – Why?
The other problem is that not only do people with celiac make antibodies against gliadin, they make antibodies against the enzyme TG2 that transforms the gliadin. (Anti-transglutaminase antibodies) They do this because gliadin is able to bind to TG2, so the body then thinks this combo is a threat, and it then attacks the TG2. This is not great as TG2 has other important roles throughout the entire body. These anti-TG antibodies have been shown to induce apoptosis (suicide) in neuronal (nerve) cells and trophoblasts (cells that form the placenta of an embryo) which explains why there is neurological damage and fertility problems in celiac disease.
The upshot of all these anti-bodies being made to gliadin and TG2 is that inflammation increases in the gut. Think of a time when you have a skin infection – you get red inflamed weeping skin. This happens in your gut. 
But wait there’s more…
Still another type of gluten peptide causes trouble for the gut cells
Yet another gluten peptide causes problems, this time though it directly ‘attacks’ the epithelial cell, which sends out stress signals, fighter cells get called in and inflammatory chemicals get sent out to try to stop the ‘attack’.
As long as gluten is eaten, the body reacts as though it is under a never ending attack, and doesn’t give up the fight
If this invader were a bacteria, our body would eventually kill them off and the attack would die down and the anti-bodies and inflammation would disappear. However in celiac disease the attacking agent can’t ever get killed off – it keeps coming and coming, as long as gluten is being eaten. So the body keeps up a never ending fight against an invader that it will never win. The loser is our own epithelium which is in a constant state of inflammation and eventually becomes damaged and non-functional. Also the more inflamed it becomes the more leaky the gut becomes and a never ending stream of pathogens can get through what should be an impenetrable barrier. The more pathogens you let through, the more fighter cells get activated, and anti-bodies can be made to a bigger range of invaders. What’s more the constant damage can eventually lead to cancer. 
The ONLY way out of this vicious cycle is to stop the attack from the primary antigen gluten. This means eating a STRICT gluten free diet for the rest of your life.
However for many with celiac disease a gluten free diet is not enough to stop the gut inflammation, and reverse the anti-bodies.
I’ll talk more about this in my next post and how to deal with it.
1. Hausch, F., et al., Intestinal digestive resistance of immunodominant gliadin peptides. American Journal of Physiology-Gastrointestinal and Liver Physiology, 2002. 283(4): p. G996-G1003.
2. Fasano, A., Intestinal Permeability and Its Regulation by Zonulin: Diagnostic and Therapeutic Implications. Clinical Gastroenterology and Hepatology, 2012. 10(10): p. 1096-1100.
3. Matysiak-Budnik, T., et al., Secretory IgA mediates retrotranscytosis of intact gliadin peptides via the transferrin receptor in celiac disease. Journal of Experimental Medicine, 2008. 205(1): p. 143-154.
4. Fasano, A. and C. Catassi, Current approaches to diagnosis and treatment of celiac disease: An evolving spectrum. Gastroenterology, 2001. 120(3): p. 636-651.
5. Klöck, C., T. DiRaimondo, and C. Khosla, Role of transglutaminase 2 in celiac disease pathogenesis. Seminars in Immunopathology, 2012. 34(4): p. 513-522.
6. Koning, F., Celiac disease: quantity matters. Seminars in Immunopathology, 2012. 34(4): p. 541-549.
7. Klöck, C., T.R. DiRaimondo, and C. Khosla, Role of transglutaminase 2 in celiac disease pathogenesis. Seminars in Immunopathology, 2012. 34(4): p. 513-522.
8. Bethune, M.T. and C. Khosla, Parallels between pathogens and gluten peptides in celiac sprue. Plos Pathogens, 2008. 4(2).
About Julianne Taylor, RN
I am passionate about the power of diet for health and fat loss. The paleo diet transformed my own health. I currently work with individuals, and deliver paleo nutrition seminars on a regular basis nation wide.
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Ketosis is an often misunderstood subject. Its presence is thought to be equal to starvation or a warning sign of something going wrong in your metabolism. But nothing could be farther from the truth, except if you are an ill-treated type 1 diabetic person. Ketones – contrary to popular belief and myth – are a much needed and essential healing energy source in our cells that comes from the normal metabolism of fat.
The entire body uses ketones in a more safe and effective way that the energy source coming from carbohydrates – sugar AKA glucose. Our bodies will produce ketones if we eat a diet devoid of carbs or a low carb diet (less than 60 grams of carbs per day). By eating a very low carb diet or no carbs at all (like a caveman) we become keto-adapted.
In fact, what is known today as the ketogenic diet was the number one treatment for epilepsy until Big Pharma arrived with its dangerous cocktails of anti-epileptic drugs. It took several decades before we heard again about this diet, thanks in part to a parent who demanded it for his 20-month-old boy with severe seizures. The boy’s father had to find out about the ketogenic diet in a library as it was never mentioned as an option by his neurologist. After only 4 days on the diet, his seizures stopped and never returned. The Charlie Foundation was born after the kid’s name and his successful recovery, but nowadays the ketogenic diet is available to the entire world and it’s spreading by word of mouth thanks to its healing effects.
It is not only used as a healthy lifestyle, it is also used for conditions such as infantile spasms, epilepsy, autism, brain tumors, Alzheimer’s disease, Lou Gehrig’s disease, depression, stroke, head trauma, Parkinson’s disease, migraine, sleep disorders, schizophrenia, anxiety, ADHD, irritability, polycystic ovarian disease, irritable bowel syndrome, gastroesophageal reflux, obesity, cardiovascular disease, acne, type 2 diabetes, tremors, respiratory failure and virtually every neurological problem but also cancer, and conditions were tissues need to recover after a loss of oxygen.
Our body organs and tissues work much better when they use ketones as a source of fuel, including the brain, heart and the core of our kidneys. If you ever had a chance to see a heart working in real time, you might have noticed the thick fatty tissue that surrounds it. In fact, heart surgeons get to see this every day. A happy beating heart is one that is surrounded by layers of healthy fat. Both the heart and the brain run at least 25% more efficiently on ketones than on blood sugar.
Ketones are the ideal fuel for our bodies unlike glucose – which is damaging, less stable, more excitatory and in fact shortens your life span. Ketones are non-glycating, which is to say, they don’t have a caramelizing aging effect on your body. A healthy ketosis also helps starve cancer cells as they are unable to use ketones for fuel, relying on glucose alone for their growth.  The energy producing factories of our cells – the mitochondria – work much better on a ketogenic diet as they are able to increase energy levels on a stable, long-burning, efficient, and steady way. Not only that, a ketogenic diet induces epigenetic changes which increases the energetic output of our mitochondria, reduces the production of damaging free radicals, and favors the production of GABA – a major inhibitory brain chemical. GABA has an essential relaxing influence and its favored production by ketosis also reduces the toxic effects of excitatory pathways in our brains. Furthermore, recent data suggests that ketosis alleviates pain other than having an overall anti-inflammatory effect. 
The ketogenic diet acts on multiple levels at once, something that no drug has been able to mimic. This is because mitochondria is specifically designed to use fat for energy. When our mitochondria uses fat as an energetic source, its toxic load is decreased, expression of energy producing genes are increased, its energetic output is increased, and the load of inflammatory energetic-end-products is decreased.
The key of these miraculous healing effects relies in the fact that fat metabolism and its generation of ketone bodies (beta-hydroxybutyrate and acetoacetate) by the liver can only occur within the mitochondrion, leaving chemicals within the cell but outside the mitochondria readily available to stimulate powerful anti-inflammatory antioxidants. The status of our mitochondria is the ultimate key for optimal health and while it is true that some of us might need extra support in the form of nutritional supplementation to heal these much needed energy factories, the diet still remains the ultimate key for a proper balance.
Our modern world’s staple energetic source is sugar which needs to be processed first in the cell soup before it can be passed into the energy factory of the cell- the mitochondrion. Energy sources from fat don’t require this processing; it goes directly into the mitochondria for energetic uses. That is, it is more complicated to create energy out of sugar than out of fat. As Christian B. Allan, PhD and Wolfgang Lutz, MD said in their book Life Without Bread:
Carbohydrates are not required to obtain energy. Fat supplies more energy than a comparable amount of carbohydrate, and low-carbohydrate diets tend to make your system of producing energy more efficient. Furthermore, many organs prefer fat for energy.
The fact is you get MORE energy per molecule of fat than sugar. How many chronic and autoimmune diseases have an energy deficit component? How about chronic fatigue? Fibromyalgia? Rheumatoid Arthritis? Multiple Sclerosis? Cancer? Back to Allan and Lutz:
Mitochondria are the power plants of the cell. Because they produce most of the energy in the body, the amount of energy available is based on how well the mitochondria are working. Whenever you think of energy, think of all those mitochondria churning out ATP to make the entire body function correctly. The amount of mitochondria in each cell varies, but up to 50 percent of the total cell volume can be mitochondria. When you get tired, don’t just assume you need more carbohydrates; instead, think in terms of how you can maximize your mitochondrial energy production…
If you could shrink to a small enough size to get inside the mitochondria, what would you discover? The first thing you’d learn is that the mitochondria are primarily designed to use fat for energy!
In short, let fat be thy medicine and medicine be thy fat!
You will think that with all of this information we would see ketogenic diets recommended right and left by our health care providers, but alas, that is not the case. Mainstream nutritionists recommend carbohydrates AKA sugar as the main staple of our diets. The problem with this (and there are several of them) is that in the presence of a high carb diet we are unable to produce ketones from the metabolism of fats, thus, depriving ours bodies from much healing ketone production. The fact that we live in a world which uses glucose as a primary fuel means that we eat a very non healing food in more ways than one.
We have been on a ketogenic diet for nearly three million years and it has made us human. It was the lifestyle in which our brains got nurtured and evolved. But not anymore, unless we all make an effort to reclaim this lost wisdom. Nowadays the human brain is not only shrinking, but brain atrophy is the norm as we age and get plagued with diseases such as Alzheimer’s disease, Parkinson’s disease, senile dementia and so forth.
In the mean time new research is starting to elucidate the key role of our mitochondria in the regulation of the cell cycle – the vital process by which a single celled fertilized egg develops into a mature organism, as well as the process by which hair, skin, blood cells, and some internal organs are renewed. In the complicated and highly choreographed events surrounding cell-cycle progression, mitochondria are not simple bystanders merely producing energy but instead are full-fledged participants. Given the significant amount of energy needed to make all the nutrients required for cell division, it makes sense that some coordination existed. This long ignored and overlooked connection between the mitochondria and the cell cycle is something that is worthy of considerable more attention as we understand the role of diet in our bodies. We’ll have to take a closer look to this subject of ketosis, as it really holds the key to unlock our transformational pathways that will lead us to an outstanding healthy living.
Mitochondria are best known as the powerhouses of our cells since they produce the cell’s energy. But they also lead the genetic orchestra which regulates how every cell ages, divides, and dies. They help dictate which genes are switched on or off in every single cell of our organism. They also provide the fuel needed to make new brain connections, repair and regenerate our bodies.
Whether we are housewives, sportsmen or labor people, energy is a topic that concerns us all, every day and in every way. Our well being, behavior and ability to perform the tasks in front of us to do is our individual measure of energy. But how we derive energy from the foods that we eat?
There are many man-made myths surrounding energy production in the body and which foods supply energy. Mainstream science says that carbohydrates are what mitochondria use as fuel for energy production. This process is called oxidative metabolism because oxygen is consumed in the process. The energy produced by mitochondria is stored in a chemical “battery”, a unique molecule called adenosine triphosphate (ATP). Energy-packed ATP can then be transported throughout the cell, releasing energy on demand of specific enzymes. In addition to the fuel they produce, mitochondria also create a by-product related to oxygen called reactive oxygen species (ROS), commonly known as free radicals. But what we are not told is that mitochondria were specifically designed to use fat for energy, not carbohydrate.
Mitochondria regulate cellular suicide, AKA apoptosis, so that old and dysfunctional cells which need to die will do so, leaving space for new ones to come into the scene. But when mitochondria function becomes impaired and send signals that tell normal cells to die, things go wrong. For instance, the destruction of brain cells leads to every single neurodegenerative condition known including Alzheimer’s disease, Parkinson’s disease and so forth. Mitochondrial dysfunction has wide-ranging implications, as the health of the mitochondria intimately affects every single cell, tissue and organ within your body.
The catalysts for this destruction is usually uncontrolled free radical production which cause oxidative damage to tissues, fat, proteins, DNA; causing them to rust. This damage, called oxidative stress, is at the basis of oxidized cholesterol, stiff arteries (rusty pipes) and brain damage. Oxidative stress is a key player in dementia as well as autism.
We produce our own anti-oxidants to keep a check on free radical production, but these systems are easily overwhelmed by a toxic environment and a high carb diet, in other words, by today’s lifestyle and diet.
Mitochondria also have interesting characteristics which differentiate them from all other structural parts of our cells. For instance, they have their own DNA (referred as mtDNA) which is separate from the widely known DNA in the nucleus (referred as n-DNA),. Mitochondrial DNA comes for the most part from the mother line, which is why mitochondria is also considered as your feminine life force. This mtDNA is arranged in a ring configuration and it lacks a protective protein surrounding, leaving its genetic code vulnerable to free radical damage. If you don’t eat enough animal fats, you can’t build a functional mitochondrial membrane which will keep it healthy and prevent them from dying.
If you have any kind of inflammation from anywhere in your body, you damage your mitochondria. The loss of function or death of mitochondria is present in pretty much every disease. Dietary and environmental factors lead to oxidative stress and thus to mitochondrial injury as the final common pathway of diseases or illnesses.
Autism, ADHD, Parkinson’s, depression, anxiety, bipolar disease, brain aging are all linked with mitochondrial dysfunction from oxidative stress. Mitochondrial dysfunction contributes to congestive heart failure, type 2 diabetes, autoimmune disorders, aging, cancer, and other diseases.
Whereas the nDNA provides the information your cells need to code for proteins that control metabolism, repair, and structural integrity of your body, it is the mtDNA which directs the production and utilization of your life energy. A cell can still commit suicide (apoptosis) even when it has no nucleus nor nDNA.
Because of their energetic role, the cells of tissues and organs which require more energy to function are richer in mitochondrial numbers. Cells in our brains, muscles, heart, kidney and liver contain thousands of mitochondria, comprising up to 40% of the cell’s mass. According to Prof. Enzo Nisoli, a human adult possesses more than ten million billion mitochondria, making up a full 10% of the total body weight. Each cell contains hundreds of mitochondria and thousands of mtDNA.
Since mtDNA is less protected than nDNA because it has no “protein” coating (histones), it is exquisitely vulnerable to injury by destabilizing molecules such as neurotoxic pesticides, herbicides, excitotoxins, heavy metals and volatile chemicals among others. This tips off the balance of free radical production to the extreme which then leads to oxidative stress damaging our mitochondria and its DNA. As a result we get overexcitation of cells and inflammation which is at the root of Parkinson’s disease and other diseases, but also mood problems and behavior problems.
Enough energy means a happy and healthy life. It also reflects in our brains with focused and sharp thinking. Lack of energy means mood problems, dementia, and slowed mental function among others. Mitochondria are intricately linked to the ability of the prefrontal cortex –our brain’s captain- to come fully online. Brain cells are loaded in mitochondria that produce the necessary energy to learn and memorize, and fire neurons harmoniously.
The sirtuin family of genes works by protecting and improving the health and function of your mitochondria. They are positively influenced by a diet that is non-glycating, i.e. a low carb diet as opposed to a high carb diet which induces mitochondrial dysfunction and formation of reactive oxygen species.
Another thing that contributes to mitochondrial dysfunction is latent viral infection such as the ones of the herpes family. As I mentioned in On Viral “Junk” DNA, a DNA Enhancing Ketogenic Diet, and Cometary Kicks, most, if not all of your “junk” DNA has viral-like properties. If a pathogenic virus takes hold of our DNA or RNA, it could lead to disease or cancer.
Herpes simplex virus is a widespread human pathogen and it goes right after our mitochondrial DNA. Herpes simplex virus establishes its latency in sensory neurons, a type of cell that is highly sensitive to the pathological effects of mt DNA damage. A latent viral infection might be driving the brain cell loss in neurodegenerative diseases such as Alzheimer’s disease. As I speculated in Heart attacks, CFS, herpes virus infection and the vagus nerve , a latent herpes virus infection might drive more diseases than we would like to admit.
Members of the herpes virus family (i.e. cytomegalovirus and Epstein-Barr virus which most people have as latent infections!), can go after our mitochondrial DNA, causing neurodegenerative diseases by mitochondrial dysfunction. But a ketogenic diet is the one thing that would help stabilize mtDNA since mitochondria runs the best on fat fuel. As it happens, Alzheimer’s disease is the one condition where a ketogenic diet has its most potential healing effect.
The role of mitochondrial dysfunction in our “modern” age maladies is a staggering one. Optimal energetic sources are essential if we are to heal from chronic ailments. It is our mitochondria which lies at the interface between the fuel from foods that come from our environment and our bodies’ energy demands. And it is a metabolism based on fat fuel, a ketone metabolism, the one which signals epigenetic changes that maximizes energetic output within our mitochondria and help us heal.
Ketosis – Closer Look
The presence of ketones in the blood and urine, a condition known as ketosis, has always been regarded as a negative situation, related to starvation. While it is true that ketones are produced during fasting, ketones are also produced in times of plenty, but not plenty of carbohydrates since a carb metabolism suppresses ketosis. In the absence of most carbs in the diet, ketones will form from fat to supply for energy. This is true even if lots of fats and enough protein are eaten, something that is hardly a starvation condition.
As we already saw, a ketogenic diet has been proved useful in a number of diseases, especially neurological ones. Strictly speaking, a ketogenic diet is a high fat diet in which carbohydrates are either completely eliminated or nearly eliminated so that the body has the very bare minimum sources of glucose. That makes fats (fatty acids) a mandatory energetic fuel source for both the brain and other organs and tissues. If you are carb intake is high, you’ll end up storing both the fat and the carbs in your fat tissue thanks to the hormone insulin. A ketogenic diet is not a high protein diet, which as it happens, can also stimulate insulin. It is basically a diet where you rely primarily on animal foods and especially their fats.
Among the by-products of fat burning metabolism are the so called ketone bodies – acetoacetate, β-hydroxybutyrate and acetone – which are produced for the most part by the liver. When our bodies are running primarily on fats, large amounts of acetyl-CoA are produced which exceed the capacity of the Krebs cycle, leading to the making of these three ketone bodies within liver mitochondria. Our levels of ketone bodies in our blood go up and the brain readily uses them for energetic purposes. Ketone bodies cross the blood brain barrier very readily. Their solubility also makes them easily transportable by the blood to other organs and tissues. When ketone bodies are used as energy, they release acetyl-CoA which then goes to the Krebs cycle again to produce energy.
In children who were treated with the ketogenic diet to treat their epilepsy, it was seen that they become seizure-free even long after the diet ended, meaning that not only did the diet proved to be protective, but also it modified the activity of the disease , something that no drug has been able to do. In Alzheimer’s disease, as levels of ketone bodies rise, memory improves. People’s starved brains finally receive the much needed fats they need! In fact, every single neurological disease is improved on the ketogenic diet.
The benefits of a ketogenic diet can be seen as fast as one week, developing gradually over a period of 3 weeks. There are several changes in gene expression involving metabolism, growth, development, and homeostasis among others.
The hippocampus is a region in your brain that is very vulnerable to stress which makes it lose its brain cells. The hippocampus has to do with memory, learning, and emotion. As it happens, a ketogenic diet promotes the codification of genes which creates mitochondria in the hippocampus, making more energy available. A larger mitochondrial load and more energy means more reserve to withstand much more stress.
In some animal models, there is a 50% increase in the total number of mitochondria in the hippocampus, resulting in more brain ATP. Other animal studies show how communication between brain cells in the hippocampus would remain smooth for 60% longer when exposed to a stressful stimulus compared to their counterparts who didn’t had a ketogenic diet. This is very important since too much stress can damage the hippocampus and its capacity to retrieve information, making you “absent-minded” or “brain-scattered”, as well as affecting the ability of your prefrontal cortex to think and manage behavior.
A ketogenic diet also increases levels of the calming neurotransmitter – GABA which then serves to calm down the overexcitation which is at the base of major neurodegenerative diseases, but also anxiety and other mood problems. A ketogenic diet also increases antioxidant pathways that level the excess production of free radicals from a toxic environment. It also enhances anti-inflammatory pathways.
Ketosis also cleans our cells from proteins that act like “debris” and which contribute to aging by disrupting a proper functioning of the cell. It basically does this by what is known as autophagy which preserves the health of cells and tissues by replacing outdated and damaged cellular components with fresh ones. This prevents degenerative diseases, aging, cancer, and protects you against microbial infections.A ketogenic diet not only rejuvenates you, it also makes a person much less susceptible to viruses and bacterial infections. This is very relevant due to the increasing number of weird viral and bacterial infections that seem to be incoming from our upper atmosphere (for more information see New Light on the Black Death: The Viral and Cosmic Connection), or due to high levels of radiation that creates more pathogenic strains (see Detoxify or Die: Natural Radiation Protection Therapies for Coping With the Fallout of the Fukushima Nuclear Meltdown). Either or, we are more vulnerable than ever due to the state of our mitochondria. But we can prepare for the worst with ketosis.
Ketone-enhanced autophagy is very important because autophagy can target viruses and bacteria that grow inside cells which are very problematical. Intracellular viruses and bacteria can lead to severe mitochondrial dysfunction and ketosis remains by far our best chance against them.
Ketone bodies production through intermittent fasting and the ketogenic diet is the most promising treatment for mitochondrial dysfunction. The longevity benefits seen caloric restriction research is due to the fact that our bodies shift to a fat burning metabolism within our mitochondria. With a ketogenic diet, we go into a fat burning metabolism without restricting our caloric intake.
Ketosis deals effectively with all the problems of a diet rich in carbs – the one recommended by mainstream science: anxiety, food cravings, irritability, tremors, and mood problems among others. It is a crime to discourage the consumption of a high fat diet considering that a ketogenic diet shrinks tumors on human and animal models, and enhances our brain’s resiliency against stress and toxicity.
In addition to increasing the production of our body’s natural valium – GABA – the increased production of acetyl-CoA generated from the ketone bodies also drives the Krebs cycle to increase mitochondrial NADH (reduced nicotinamide adenine nucleotide) which our body uses in over 450 vital biochemical reactions – including the cell signaling and assisting of the ongoing DNA repair. Because the ketone body beta-hydroxybutyrate is more energy rich than pyruvate, it produces more ATP. Ketosis also enhances the production of important anti-oxidants that deal with toxic elements from our environments, including glutathione.
Mitochondria from the hippocampus of ketogenic diet-fed animals are also resistant to mtDNA damage and are much less likely to commit cell suicide –apoptosis- at inappropriate times.
As Douglas C. Wallace, PhD, Director of the Center for Mitochondrial and Epigenomic Medicine says, “the ketogenic diet may act at multiple levels: It may decrease excitatory neuronal activity, increase the expression of bioenergetic genes, increase mitochondrial biogenesis and oxidative energy production, and increase mitochondrial NADPH production, thus decreasing mitochondrial oxidative stress.”
Keto-adaptation results in marked changes in how we construct and maintain optimum membrane (“mem-brain”) composition, not only because of the healthy fats we provide through the diet, but also because of less free radical production and inflammatory mediators, along with more production of anti-oxidants. It is really the ideal balanced state.
Moreover, you might want to keep in mind this excerpt from Human Brain Evolution: The Influence of Freshwater and Marine Food Resources:
There are two key advantages to having ketone bodies as the main alternative fuel to glucose for the human brain. First, humans normally have significant body fat stores, so there is an abundant supply of fatty acids to make ketones. Second, using ketones to meet part of the brain’s energy requirement when food availability is intermittent frees up some glucose for other uses and greatly reduces both the risk of detrimental muscle breakdown during glucose synthesis, as well as compromised function of other cells dependent on glucose, that is, red blood cells. One interesting attribute of ketone uptake by the brain is that it is four to five times faster in newborns and infants than in adults. Hence, in a sense, the efficient use of ketones by the infant brain means that it arguably has a better fuel reserve than the adult brain. Although the role of ketones as a fuel reserve is important, in infants, they are more than just a reserve brain fuel – they are also the main substrate for brain lipid synthesis.
I have hypothesized that evolution of a greater capacity to make ketones coevolved with human brain expansion. This increasing capacity was directly linked to evolving fatty acid reserves in body fat stores during fetal and neonatal development. To both expand brain size and increase its sophistication so remarkably would have required a reliable and copious energy supply for a very long period of time, probably at least a million, if not two million, years. Initially, and up to a point, the energy needs of a somewhat larger hominin brain could be met by glucose and short – term glucose reserves such as glycogen and glucose synthesis from amino acids. As hominins slowly began to evolve larger brains after having acquired a more secure and abundant food supply, further brain expansion would have depended on evolving significant fat stores and having reliable and rapid access to the fuel in those fat stores. Fat stores were necessary but were still not sufficient without a coincident increase in the capacity for ketogenesis. This unique combination of outstanding fuel store in body fat as well as rapid and abundant availability of ketones as a brain fuel that could seamlessly replace glucose was the key fuel reserve for expanding the hominin brain, a reserve that was apparently not available to other land – based mammals, including nonhuman primates.
It is indisputable that a ketogenic diet has protective effects in our brains. With all the evidence of its efficacy in mitochondrial dysfunction, it can be applied for all of us living in a highly stressful and toxic environment. Ketone bodies are healing bodies that helped us evolve and nowadays our mitochondria are always busted in some way or another since the odds in this toxic world are against us. Obviously, there are going to be people with such damaged mtDNA or with mutations they were born with, who can’t modify their systems (i.e. defects on L-carnitine metabolism), but even in some of those cases, they can halt or slow down further damage. Our healthy ancestors never had to deal with the levels of toxicity that we live nowadays and nevertheless, they ate optimally. Considering our current time and environment, the least we can do is eat optimally for our physiology.
The way to have healing ketone bodies circulating in our blood stream is to do a high fat, restricted carb and moderated protein diet. Coupled with intermittent fasting which will enhance the production of ketone bodies, and resistance training which will create mitochondria with healthier mtDNA, we can beat the odds against us.
What is considered nowadays a “normal diet” is actually an aberration based on the corruption of science which benefits Big Agra and Big Pharma. If we would go back in time to the days before the modern diet became normalized by corporative and agricultural interests, we will find that ketosis was the normal metabolic state. Today’s human metabolic state is aberrant. It is time to change that.
 A research member of sott.net’s forum has diabetes type 1 and is doing the ketogenic diet. On normal circumstances, diabetics (including type I) report amazing results on a low-carbohydrate diet. See Dr. Bernstein’s Diabetics Solution by Richard K. Bernstein, MD (Little, Brown and Company: 2007).
 It varies among each person, but the general range is between 0 and 70 grams of carbs plus moderate intake of protein, between 0.8 and 1.5 grams of protein per kg of ideal body weight. Pregnant women and children should not have their protein restricted.
 Ketogenic diets in seizure control and neurologic disorders by Eric Kossoff, MD, Johns Hopkins Hospital, Baltimore, Maryland. The Art and Science of Low Carbohydrate Living by Jeff S. Volek, PhD, Rd and Stephen D. Phinney, MD, PhD. Beyond Obesity, LLC , 2011.
A Paoli, A Rubini, J S Volek and K A Grimaldi. Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets. European Journal of Clinical Nutrition (2013) 67, 789–796
 Rainer J Klement, Ulrike Kämmerer. Is there a role for carbohydrate restriction in the treatment and prevention of cancer? Nutr Metab (Lond). Oct 26, 2011; 8: 75.
 If the genetic code is the hardware for life, the epigenetic code is software that determines how the hardware behaves.
 David N. Ruskin and Susan A. Masino, The Nervous System and Metabolic Dysregulation: Emerging Evidence Converges on Ketogenic Diet Therapy. Front Neurosci. 2012; 6: 33.
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 Hipkiss AR. Energy metabolism, altered proteins, sirtuins and ageing: converging mechanisms? Biogerontology. 2008 Feb;9(1):49-55.
 Saffran HA, Pare JM, Corcoran JA, et al. Herpes simplex virus eliminates host mitochondrial DNA. EMBO Rep. 2007 Feb;8(2):188-93.
 Porcellini E, Carbone I, et al. Alzheimer’s disease gene signature says: beware of brain viral infections. Immun Ageing. 2010 Dec 14;7:16.
 Gasior M, Rogawski MA, Hartman AL. Neuroprotective and disease-modifying effects of the ketogenic diet. Behav Pharmacol. 2006 Sep;17(5-6):431-9.
 Maalouf M, Rho JM, Mattson MP. The neuroprotective properties of calorie restriction, the ketogenic diet, and ketone bodies. Brain Res Rev. 2009 Mar;59(2):293-315.
 Nylen K, Velazquez JL. The effects of a ketogenic diet on ATP concentrations and the number of hippocampal mitochondria in Aldh5a1(-/-) mice. Biochim Biophys Acta. 2009 Mar;1790(3):208-12.
 Bough K. Energy metabolism as part of the anticonvulsant mechanism of the ketogenic diet. Epilepsia. 2008 Nov;49 Suppl 8:91-3.
 Finn PF, Dice JF. Ketone bodies stimulate chaperone-mediated autophagy. J Biol Chem. 2005 Jul 8;280(27):25864-70.
 Yuk JM, Yoshimori T, Jo EK. Autophagy and bacterial infectious diseases. Exp Mol Med. 2012 Feb 29;44(2):99-108.
 Chandra Wickramasinghe, Milton Wainwright & Jayant Narlika. SARS – a clue to its origins? The Lancet, vol. 361, May 23, 2003, pp 1832.
 Yordy B, Iwasaki A. Autophagy in the control and pathogenesis of viral infection. Curr Opin Virol. 2011 Sep;1(3):196-203.
 Douglas C. Wallace, Weiwei Fan, and Vincent Procaccio. Mitochondrial Energetics and Therapeutics Annu Rev Pathol. 2010; 5: 297–348.
 Stephen Cunnane, Kathlyn Stewart.Human Brain Evolution: The Influence of Freshwater and Marine Food Resources. June 2010, Wiley-Blackwell.
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WE like the idea that food can be the answer to our ills, that if we eat nutritious foods we won’t need medicine or supplements. We have valued this notion for a long, long time. The Greek physician Hippocrates proclaimed nearly 2,500 years ago: “Let food be thy medicine and medicine be thy food.” Today, medical experts concur. If we heap our plates with fresh fruits and vegetables, they tell us, we will come closer to optimum health.
This health directive needs to be revised. If we want to get maximum health benefits from fruits and vegetables, we must choose the right varieties. Studies published within the past 15 years show that much of our produce is relatively low in phytonutrients, which are the compounds with the potential to reduce the risk of four of our modern scourges: cancer, cardiovascular disease, diabetes and dementia. The loss of these beneficial nutrients did not begin 50 or 100 years ago, as many assume. Unwittingly, we have been stripping phytonutrients from our diet since we stopped foraging for wild plants some 10,000 years ago and became farmers.
These insights have been made possible by new technology that has allowed researchers to compare the phytonutrient content of wild plants with the produce in our supermarkets. The results are startling.
Wild dandelions, once a springtime treat for Native Americans, have seven times more phytonutrients than spinach, which we consider a “superfood.” A purple potato native to Peru has 28 times more cancer-fighting anthocyanins than common russet potatoes. One species of apple has a staggering 100 times more phytonutrients than the Golden Delicious displayed in our supermarkets.
Were the people who foraged for these wild foods healthier than we are today? They did not live nearly as long as we do, but growing evidence suggests that they were much less likely to die from degenerative diseases, even the minority who lived 70 years and more. The primary cause of death for most adults, according to anthropologists, was injury and infections.
Each fruit and vegetable in our stores has a unique history of nutrient loss, I’ve discovered, but there are two common themes. Throughout the ages, our farming ancestors have chosen the least bitter plants to grow in their gardens. It is now known that many of the most beneficial phytonutrients have a bitter, sour or astringent taste. Second, early farmers favored plants that were relatively low in fiber and high in sugar, starch and oil. These energy-dense plants were pleasurable to eat and provided the calories needed to fuel a strenuous lifestyle. The more palatable our fruits and vegetables became, however, the less advantageous they were for our health.
The sweet corn that we serve at summer dinners illustrates both of these trends. The wild ancestor of our present-day corn is a grassy plant called teosinte. It is hard to see the family resemblance. Teosinte is a bushy plant with short spikes of grain instead of ears, and each spike has only 5 to 12 kernels. The kernels are encased in shells so dense you’d need a hammer to crack them open. Once you extract the kernels, you wonder why you bothered. The dry tidbit of food is a lot of starch and little sugar. Teosinte has 10 times more protein than the corn we eat today, but it was not soft or sweet enough to tempt our ancestors.
Over several thousand years, teosinte underwent several spontaneous mutations. Nature’s rewriting of the genome freed the kernels of their cases and turned a spike of grain into a cob with kernels of many colors. Our ancestors decided that this transformed corn was tasty enough to plant in their gardens. By the 1400s, corn was central to the diet of people living throughout Mexico and the Americas.
When European colonists first arrived in North America, they came upon what they called “Indian corn.” John Winthrop Jr., governor of the colony of Connecticut in the mid-1600s, observed that American Indians grew “corne with great variety of colours,” citing “red, yellow, blew, olive colour, and greenish, and some very black and some of intermediate degrees.” A few centuries later, we would learn that black, red and blue corn is rich in anthocyanins. Anthocyanins have the potential to fight cancer, calm inflammation, lower cholesterol and blood pressure, protect the aging brain, and reduce the risk of obesity, diabetes and cardiovascular disease.
EUROPEAN settlers were content with this colorful corn until the summer of 1779 when they found something more delectable — a yellow variety with sweeter and more tender kernels. This unusual variety came to light that year after George Washington ordered a scorched-earth campaign against Iroquois tribes. While the militia was destroying the food caches of the Iroquois and burning their crops, soldiers came across a field of extra-sweet yellow corn. According to one account, a lieutenant named Richard Bagnal took home some seeds to share with others. Our old-fashioned sweet corn is a direct descendant of these spoils of war.
Up until this time, nature had been the primary change agent in remaking corn. Farmers began to play a more active role in the 19th century. In 1836, Noyes Darling, a onetime mayor of New Haven, and a gentleman farmer, was the first to use scientific methods to breed a new variety of corn. His goal was to create a sweet, all-white variety that was “fit for boiling” by mid-July.
He succeeded, noting with pride that he had rid sweet corn of “the disadvantage of being yellow.”
The disadvantage of being yellow, we now know, had been an advantage to human health. Corn with deep yellow kernels, including the yellow corn available in our grocery stores, has nearly 60 times more beta-carotene than white corn, valuable because it turns to Vitamin A in the body, which helps vision and the immune system.
SUPERSWEET corn, which now outsells all other kinds of corn, was derived from spontaneous mutations that were selected for their high sugar content. In 1959, a geneticist named John Laughnan was studying a handful of mutant kernels and popped a few into his mouth. He was startled by their intense sweetness. Lab tests showed that they were up to 10 times sweeter than ordinary sweet corn.
Mr. Laughnan was not a plant breeder, but he realized at once that this mutant corn would revolutionize the sweet corn industry. He became an entrepreneur overnight and spent years developing commercial varieties of supersweet corn. His first hybrids began to be sold in 1961.
Within one generation, the new extra sugary varieties eclipsed old-fashioned sweet corn in the marketplace. Build a sweeter fruit or vegetable — by any means — and we will come. Today, most of the fresh corn in our supermarkets is extra-sweet. The kernels are either white, pale yellow, or a combination of the two. The sweetest varieties approach 40 percent sugar, bringing new meaning to the words “candy corn.” Only a handful of farmers in the United States specialize in multicolored Indian corn, and it is generally sold for seasonal decorations, not food.
We’ve reduced the nutrients and increased the sugar and starch content of hundreds of other fruits and vegetables. How can we begin to recoup the losses?
Here are some suggestions to get you started. Select corn with deep yellow kernels. To recapture the lost anthocyanins and beta-carotene, cook with blue, red or purple cornmeal, which is available in some supermarkets and on the Internet. Make a stack of blue cornmeal pancakes for Sunday breakfast and top with maple syrup.
In the lettuce section, look for arugula. Arugula, also called salad rocket, is very similar to its wild ancestor. Some varieties were domesticated as recently as the 1970s, thousands of years after most fruits and vegetables had come under our sway. The greens are rich in cancer-fighting compounds called glucosinolates and higher in antioxidant activity than many green lettuces.
Scallions, or green onions, are jewels of nutrition hiding in plain sight. They resemble wild onions and are just as good for you. Remarkably, they have more than five times more phytonutrients than many common onions do. The green portions of scallions are more nutritious than the white bulbs, so use the entire plant. Herbs are wild plants incognito. We’ve long valued them for their intense flavors and aroma, which is why they’ve not been given a flavor makeover. Because we’ve left them well enough alone, their phytonutrient content has remained intact.
Experiment with using large quantities of mild-tasting fresh herbs. Add one cup of mixed chopped Italian parsley and basil to a pound of ground grass-fed beef or poultry to make “herb-burgers.” Herbs bring back missing phytonutrients and a touch of wild flavor as well.
The United States Department of Agriculture exerts far more effort developing disease-resistant fruits and vegetables than creating new varieties to enhance the disease resistance of consumers. In fact, I’ve interviewed U.S.D.A. plant breeders who have spent a decade or more developing a new variety of pear or carrot without once measuring its nutritional content.
We can’t increase the health benefits of our produce if we don’t know which nutrients it contains. Ultimately, we need more than an admonition to eat a greater quantity of fruits and vegetables: we need more fruits and vegetables that have the nutrients we require for optimum health.
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Melatonin is a hormone produced by the body that regulates many physiological processes.
MELATONIN supplementation is a controversial issue and I hope to help readers understand the facts so that they are not misled by wild claims.
Melatonin is a hormone produced by the pineal gland, which is situated at the base of the brain. Although this hormone is best known for regulating the sleep and wake cycles, it also plays many other important roles in the body, including maintaining a healthy immune system, serving as an antioxidant, and regulating the menstrual cycle.
Functions of melatonin
Let’s look at the functions of melatonin in greater detail. Like all hormones, melatonin sends chemical messages to various parts of the body and tells the different organs or tissues to produce more hormones or carry out certain tasks. Without melatonin, other hormonal activity in the body would be interrupted.
Production of melatonin is stimulated by darkness and inhibited by light. This is what makes the pineal gland our “internal clock”, as it controls our body’s circadian rhythm – our body’s own 24-hour time-keeping system that plays an important role in when we fall asleep and when we wake up.
It may sound like a simple function, but if this internal clock is disrupted, many other neuroendocrine functions go haywire. The body’s internal functions, as well as mental well-being, can be adversely affected. For example, you may find yourself unable to think clearly, and forget key facts if your melatonin production is upset.
Children and healthy young adults have higher levels of melatonin. As they advance beyond middle-age, the amount of melatonin produced by the body decreases. This may explain why elderly adults tend to have difficulty sleeping at night.
The level of melatonin in the blood appears to trigger the adrenal glands to increase or suppress the secretion of male and female sex hormones. In this respect, it controls the timing and release of reproductive hormones in a woman’s body. It is instrumental in determining when menstruation begins, how long the cycle lasts, and when menopause occurs.
Melatonin also affects the production of pituitary gland hormones, including human growth hormone. This hormone plays a role in muscle and bone growth, as well as energy metabolism, among other essential functions.
Finally, it is believed that the immune system can be strengthened by melatonin. This is because melatonin is recognised as a strong antioxidant, which is a substance that protects your cells from the effects of free radicals. Free radicals are molecules produced when your body breaks down food, or are generated through environmental exposure to tobacco smoke and radiation.
Free radicals can damage cells, and may play a role in heart disease, cancer, and other diseases.
There is a theory that melatonin levels in the population are decreasing because of light “pollution”. This phenomenon, also called urban sky glow, is where the sky is unnaturally bright at night due to artificial lighting from highways, streets, malls, stadiums and homes.
A study published in 2007 in the Journal of Pineal Research stated that exposure to low-level incandescent lightning for only 39 minutes can suppress melatonin levels by up to 50%.
Benefits of melatonin
Sleep is as important as food and air, and the quantity and quality an individual gets is also extremely important. According to data from the Cancer Prevention Study II, individuals who average seven hours of sleep each night have a lower mortality rate than do those who sleep eight hours or more.
Interestingly, research shows that sleeping more than eight hours may have deleterious effects, although the reasons for this are less clear.
A paper recently published in Neuroendocrinology Letters says that disruption of the circadian rhythms caused by over-exposure to light at night – because of both night work and as a personal choice and lifestyle – has been associated with cancer in humans. And there’s evidence of increased breast and colon cancer risk in shift workers.
Melatonin is most popularly known in its supplement form, which is touted for all sorts of conditions, ranging from sleep disturbance to anti-cancer and anti-ageing effects.
There is still a lot of debate within medical and health circles about the safety and efficacy of melatonin supplements. As melatonin is a hormone, you should be very cautious about taking such supplements.
Below, I will describe some of the common claims made by proponents of melatonin supplements. Many are still not validated by indisputable scientific evidence, so be sure to always ask your doctor’s advice first.
Sleep disturbance is the most common reason why people seek out melatonin supplements. In many cases, it is due to external factors, such as jet lag or shift work. Jet lag occurs when you cross time zones during long-distance travel, so night becomes day and day becomes night for you.
Shift workers also have trouble regulating their circadian rhythms because they go to sleep in the daytime, but the bright daylight disrupts their melatonin production.
Some people suffer from insomnia, which is the inability to fall asleep or remain asleep for a reasonable period during the night. Melatonin supplements are believed to be able to induce sleep in these people who either have low melatonin levels or have had their internal clocks disrupted.
Melatonin supplements are also claimed to be powerful antioxidants that help protect us from infection, inflammation, and act as immune enhancers because the immune system works less efficiently as we age.
Melatonin has also been shown to be beneficial for Alzheimer’s disease, especially for coping with the period called “sundowning”, when patients become agitated during late afternoon and early evening; gastric ulcers; hot flashes in menopausal women because melatonin suppresses luteinizing hormone (LH) in postmenopausal women; cardiovascular disease, since melatonin helps regulate nitric oxide production, which plays a vital role in ensuring proper cardiovascular function; and also for attention deficit disorder and insomnia in children.
Some small studies have looked at the use of melatonin to reduce high blood pressure, enhance the efficacy of cancer treatment, and reduce radiation-induced side effects in cancer treatment.
And in studies done on animals, it has been shown to improve immunity and extend lifespan by 20%.
Melatonin supplementation is not to be taken without care. Aside from the fact that there is no conclusive scientific evidence to support its long-term use, it can also have unpleasant side effects for some people.
Some people have reported vivid dreams or nightmares when they take melatonin. Its sleep-inducing effects may also extend into the daytime and cause drowsiness during the day. It is best to avoid driving or operating machinery if you are taking melatonin.
You should also be aware of other side effects, such as stomach cramps, dizziness, headache, irritability, decreased libido, as well as breast enlargement and decreased sperm count in men.
A word of caution for women: melatonin could interfere with fertility. It also should not be taken by pregnant or breastfeeding women, who are already producing abundant melatonin in their bodies.
Children and teenagers also have ample melatonin in their bodies, so supplementation could lead to overdose.
If you take certain antidepressants, such as Prozac or Nardil, do not take melatonin supplements, as both medications could interact to cause a stroke or heart attack.
Before deciding to take melatonin supplements, you can try to look for natural sources of melatonin to increase the level of the hormone in your body.
Melatonin is found in some foods, although in small amounts. Oats, sweet corn and rice are rich in melatonin, as are ginger, tomatoes, bananas and barley.
If, like many other people, you resort to melatonin supplementation for sleep problems, then you could try the following methods first to regulate your sleep cycle:
● Get eight to nine hours sleep per night.
● Get to bed by 10:30pm each night.
● Sleep in a comfortable bed – make sure the mattress is not too saggy, too hard, or creaky.
● Make your sleep and wake times the same each day, even on weekends.
● Avoid exposure to bright lights, directly before and during sleep.
● Avoid TV and reading before bed, as both stimulate the brain.
● Make your room completely dark, especially if you are a shift worker who sleeps in the daytime. Use dark curtains to block out sunlight.
● Avoid taking stimulants, like coffee, cigarettes or alcohol, before bed.
● Keep the bedroom at a comfortable temperature, not too warm or too cold.
● Avoid electromagnetic fields in the bedroom, such as TVs, clocks, radios and lights. If you must have them in the room, move them far away from the bed.
● Avoid eating before sleep.
● Move the clock out of sight and avoid loud alarm clocks.
● Try keeping a journal – write down your thoughts before sleeping, so that they are not racing through your mind.
● Limit drug use – some prescription and over-the-counter medications can inhibit sleep.
● Exercising can release stress and help you sleep better at night – but don’t exercise too close to bedtime as the body needs time to relax.
● Take a hot bath or shower before bed.
● Keep your work out of the bedroom, so that your body doesn’t recognise it as a stressful environment.
Many people will claim that melatonin supplements are safe because they are “natural”. However, everything carries potential risks and side effects, especially if you do not know whether the manufacturers are to be trusted.
Whether you need help sleeping through the night, feeling good while traveling across time zones, or just want to boost your immunity, and possibly add some years to your life, always check with your doctor before taking melatonin supplements. Tell her about your other health conditions and medications, so that you can avoid any adverse complications.
■ Datuk Dr Nor Ashikin Mokhtar is a consultant obstetrician & gynaecologist (FRCOG, UK). For further information, visit www.primanora.com. The information provided is for educational and communication purposes only and it should not be construed as personal medical advice. Information published in this article is not intended to replace, supplant or augment a consultation with a health professional regarding the reader’s own medical care.