Wat te eten voor het schoonmaken van de mitochondria?
Deze site is opgericht door een zeer tevreden cliŽnt van het Biologisch Medisch Centrum

Biologisch Medisch Centrum
HINTS
ATP energie
Behandeling CVS/ME
Dr Myhill
Dr Teitelbaum
Dr Meirleir
Dr Cheney
Dr Chia
Arts Paul van Meerendonk

ADP-ATP efficiency
Mitochondrial dysfunction
Cvs en fibromyalgie
Virus en DNA
Viruses and mitochondria
Virussen en immuunsysteem
Zware metalen

Cadmium
CVS ME aantoonbaar
CVS legitiem
esme
Research direction

Glutathion
Carnitine
D-ribose
Vitamine B12
Vitamine D
Nac
FIR
EPD Desensibilisatie
Oxymatrine
Gc MAF
CT
Meetresultaten 1

Meetresultaten 2
Meetresultaten 3
Meetresultaten 4

 

Eiwitten eten voor het schoonmaken van de mitochondria. Verzadigde vetten eten voor het verkrijgen van oxidatie bestendige veten in de mitochondria.
Minder carbohydraad eten voor het schoonmaken van de mitochondria.
Met het verbranden van vetten in de mitochondria komt er veel minder beschadigende oxidanten vrij dan met het verbranden van koolhydraten. Mitochondria herstellen beter.

 

 

 


Sulforafaan eten om de antioxidanten op de plaats te krijgen waar het werkt: in de mitochondria.

Verzadigde vetten:        melkvet, vet van vlees, cocosnoot, palmolie en chocolade.
Sulforafaan:                  broccoli, spruiten, koolsoorten
Eiwitten:                        vlees, vis, melk, kaas en eieren

carbohydraad weinig:    suiker brood pasta aardappel rijst

 

Metabolism and ketosis

The primary goal of our metabolic system is to provide fuels in the amounts needed at the times needed to keep us alive and functioning. As long as weíve got plenty of food, the metabolic systems busies itself with allocating it to the right places and storing whatís left over. In a society such as ours, there is usually too much food so the metabolic system has to deal with it in amounts and configurations that it wasnít really designed to handle, leading to all kinds of problems. But thatís a story for another day.

If you read any medical school biochemistry textbook, youíll find a section devoted to what happens metabolically during starvation. If you read these sections with a knowing eye, youíll realize that everything discussed as happening during starvation happens during carbohydrate restriction as well. There have been a few papers published recently showing the same thing: the metabolism of carb restriction = the metabolism of starvation. I would maintain, however, based on my study of the Paleolithic diet, that starvation and carb restriction are simply the polar ends of a continuum, and that carb restriction was the norm for most of our existence as upright walking beings on this planet, making the metabolism of what biochemistry textbook authors call starvation the Ďnormalí metabolism.

So, bearing in mind that carb restriction and starvation are opposite ends of the same stick and that what applies to one applies to the other, letís look at how it all works. Iíll explain it from a starvation perspective, but all the mechanisms work the same for a carb-restricted diet.

During starvation the primary goal of the metabolic system is to provide enough glucose to the brain and other tissues (the red blood cells, certain kidney cells, and others) that absolutely require glucose to function. Which makes sense if you think about it. Youíre a Paleolithic man or woman, youíre starving, youíve got to find food, you need a brain, red blood cells, etc. to do it. Youíve got to be alert, quick on your feet, and not focused on how hungry you are.

If youíre not eating or if youíre on a low-carbohydrate diet, where does this glucose come from?

If youíre starving, glucose comes mainly from one place, and that is from the bodyís protein reservoir: muscle. A little can come from stored fat, but not from the fatty acids themselves. Although glucose can be converted to fat, the reaction canít go the other way. Fat is stored as a triglyceride, which is three fatty acids hooked on to a glycerol molecule. The glycerol molecule is a three-carbon structure that, when freed from the attached fatty acids, can combine with another glycerol molecule to make glucose. Thus a starving person can get a little glucose from the fat that is released from the fat cells, but not nearly enough. The lionís share has to come from muscle that breaks down into amino acids, several of which can be converted by the liver into glucose. (There are a few other minor sources of glucose conversion: the Cori cycle, for example, but these are not major sources, so weíll leave them for another, more technical, discussion.)

But the breakdown of muscle creates another problem, namely, that (in Paleolithic times and before) survival was dependent upon our being able to hunt down other animals and/or forage for plant foods. It makes it tough to do this if a lot of muscle is being converted into glucose and your muscle mass is dwindling.

The metabolic system is then presented with two problems: 1) getting glucose for the glucose-dependent tissues; and 2) maintaining as much muscle mass as possible to allow hunting and foraging to continue.

Early on, the metabolic system doesnít know that the starvation is going to go on for a day or for a week or two weeks. At first it plunders the muscle to get its sugar. And remember from a past post that a normal blood sugar represents only about a teaspoon of sugar dissolved in the entire blood volume, so keeping the blood sugar normal for a day or so doesnít require a whole lot of muscular sacrifice. If we figure that an average person requires about 200 grams of sugar per day to meet all the needs of the glucose-dependent tissues, weíre looking at maybe a third of a pound of muscle per day, which isnít all that big a deal over the first day. But we wouldnít want it to continue at that rate. If we could reduce that amount and allow our muscle mass to last as long as possible, it would be a big help.

The metabolic system could solve its problem by a coming up with a way to reduce the glucose-dependent tissuesí need for glucose so that the protein could be spared as long as possible.

Ketones to the rescue.

The liver requires energy to convert the protein to glucose. The energy comes from fat. As the liver breaks down the fat to release its energy to power gluconeogenesis, the conversion of protein to sugar, it produces ketones as a byproduct. And what a byproduct they are. Ketones are basically water soluble (meaning they dissolve in blood) fats that are a source of energy for many tissues including the muscles, brain and heart. In fact, ketones act as a stand in for sugar in the brain. Although ketones canít totally replace all the sugar required by the brain, they can replace a pretty good chunk of it. By reducing the bodyís need for sugar, less protein is required, allowing the muscle mass (the protein reservoir) to last a lot longer before it is depleted. And ketones are the preferred fuel for the heart, making that organ operate at about 28 percent greater efficiency.

Fat is the perfect fuel. Part of it provides energy to the liver so that the liver can convert protein to glucose. The unusable part of the fat then converts to ketones, which reduce the need for glucose and spare the muscle in the process.

If, instead of starving, youíre following a low-carb diet, it gets even better. The protein you eat is converted to glucose instead of the protein in your muscles. If you keep the carbs low enough so that the liver still has to make some sugar, then you will be in fat-burning mode while maintaining your muscle mass, the best of all worlds. How low is low enough? Well, when the ketosis process is humming along nicely and the brain and other tissues have converted to ketones for fuel, the requirement for glucose drops to about 120-130 gm per day. If you keep your carbs below that at, say, 60 grams per day, youíre liver will have to produce at least 60-70 grams of glucose to make up the deficit, so you will generate ketones that entire time.

So, on a low-carb diet you can feast and starve all at the same time. Is it any wonder itís so effective for weight loss?

 


Ketosis cleans our cells

 

In going through and catching up on all the online issues of Science, I finally reached the most current issue, which contains an article of interest. Originally published in 1970 in the journal Nature, this article was featured in the current issue of Sage KE, an anti-aging supplement to Science, as a blast from the past in their Classic Papers section. The paper was the first to show that the accumulation of non-functional, or junk, proteins play a role in the aging process. This article caught my eye because of another I had read recently and had touched upon in a previous post.

Anti-aging scientists are now pretty sure that one of the forces behind the aging and senescence process is the junk protein matter that accumulates in the cells, hampering cellular function. If the junk builds up enough, it basically crowds out the working part of the cell, killing the cell off in the process. As this inexorable process proceeds, more and more cells function less and less well until we, as a being, cease to function. There are other processes driving the aging function besides this accumulation of cellular debris, but if we can make some headway with cleaning out the junk, then we should be able to make the cells, and by extension us, function better for longer.

We have little chemically-operated waste disposal systems in our cells called lysosomes. Cellular debris that gets hauled to the lysosomes and dumped in gets degraded into individual amino acids, which are released into the circulation and used to re-synthesize other, functional, proteins. The process of transporting the junk proteins to the lysosomes is handled by enzymes designed for that purpose found within the cells. As long as the enzymes are working up to snuff, the junk doesnít accumulate. But as the Nature paper shows, the aging process takes its toll. Random errors in protein synthesis of these enzymes due to the aging process means that some end up being functional while others arenít. The non-functional enzymes then not only donít help haul the junk to the lysosomes, they themselves become junk. Itís easy to see whatís going to happen as time marches on.

But how can we slow this process and de-junk our cells?

Stay in ketoses a lot of the time. How do we stay in ketosis? By following a low-carbohydrate diet.

How does ketosis help us de-junk our cells?

A paper was published in the Journal of Biological Chemistry last year that tells the story. Ketones stimulate the process of chaperone-mediated autophagy (CMA). What is CMA? It is

a cellular process that allows cells to remove proteins, organelles, and foreign bodies from the cytosol [the watery interior of the cell] and deliver them to the lysosomes for degradation.

Why would the body be designed for ketones to stimulate CMA? Simple. Ketosis is one of the signs of long term starvation. Ketones are produced throughout the day and are perfectly normal, but sustained ketosis takes place during starvation and sends a message that the body needs to conserve both glucose and protein. The body begins to conserve glucose by signaling to many of the organs and tissues to start using ketones for energy instead of glucose. The body conserves protein by decreasing its use of glucose because in the absence of dietary carbohydrate (as in starvation) the body makes glucose out of protein. Conserving glucose by switching to ketones allows the body can preserve its protein stores. The other thing the body can do is to make sure that the protein it does break down to use for glucose formation comes from non-essential sources. What more non-essential source can we have than useless junk proteins floating around in the cells?

The ketones themselves stimulate the process of CMA to salvage all the junk protein to be used for glucose conversion. Ainít nature great?

Now, all we have to do to slow the aging process is to stay in some degree of ketosis most of the time and let nature take her course and clean all the junk out of our cellular attics. How do we do that? Easy. Keep our carbohydrate intake at (or preferably below) 100 grams or so per day. Why that particular number? Letís figure.

It takes about 200 grams of carbohydrate per day to provide glucose for all the structures in the body that require it. After a period of low-carbohydrate intake or starvation that amount required drops to about 130 grams per day because about 70 grams are replaced by ketones. We never really get below that because certain cells canít convert totally to ketone use and continue to require some glucose. For instance, the red blood cells must use glucose for energy as do some cells in the kidneys and the brain and central nervous system. But not to worry, the liver can easily make 200 plus grams of sugar per day to ensure that these tissues get all they need. But the liver makes most of this glucose via a process called gluconeogenesis (the generation of Ďnewí glucose) out of protein.

So, if we decrease our carbohydrate intake to below, say, 50 grams per day, the amount advised in Protein Power and other enlightened books on carb restriction, weíre in a deficit to the tune of about 150 grams per day. No problema. The liver makes up the deficit out of protein. As we start making ketones to replace the glucose, the deficit drops to about 80 grams per day, which the liver can easily provide. But here is the neat part. Most of the glucose the liver makes wonít really come from protein from our tissues; it will come from the protein we eat. Weíre not starving; weíre eating a high-protein diet. So we have plenty of protein to make glucose as we need it without robbing our muscles and other protein tissues that would get pillaged were we really starving.

But, deep in the bowels of our cells this fact is unknown. All the cells know is that ketones are all over the place, which is the signal to start the CMA process to break up junk protein.

We end up losing body fat, which is both burned for energy and converted to ketones to replace glucose, while at the same time we maintain our needed protein structures because weíre eating protein, and we de-gunk our cells. All while eating steak and eggs and lambchops and ham andÖ

It just one more reason the low-carb diet rules.


Hoe antioxidanten in de mitochondria te krijgen?

We know that free radicals cause damage, we know that the accumulation of free-radical damage is one of the major causes of aging, we know that in a test tube antioxidants neutralize free radicals, so why donít we live longer when we take antioxidants?

First, when we take antioxidant supplements they go into our blood. Most of the free radicals and free radical damage isnít in the blood. Itís deep within the mitochondria, the little sausage shaped organelles that are the power-generators within mitochondria.jpgthe cells. The supplements we take donít make it into the mitochondria, so theyíre not really effective in protecting them. If mitochondria get severely enough damaged, they die. If cells lose their mitochondria, they lose their power source, and they die. When enough cells die, we die.

Before we can understand how free radicals are created, we need to understand what happens to the food we eat. We know that food provides us with the energy we need to live, but most people donít really understand how we use the food we eat. When we eat a steak, how do we use the energy contained in the steak to power ourselves? We use it to convert ADP into ATP. ATP (adenosine triphosphate) is the energy currency of the body. It is a molecule with high-energy phosphate bonds that when cleaved release the energy required to operate all of the bodyís functions. ADP (adenosine diphosphate) is converted to ATP in the mitochondria. Energy is required for this process, and that energy comes from food.

Various metabolic pathways break down the food we eat and reduce it to high-energy electrons that end up in the mitochondria. These electrons are passed along from one complicated molecular structure to another along the inner mitochondrial membrane until they are finally handed off to oxygen, the ultimate electron receptor. (Iím really simplifying this process; entire books are written about it. Iím just giving you the most basic gist.) As these electrons are handed off from one complex to another, the energy they release during the transfer moves protons (hydrogen ions: H+) across this inner mitochondrial membrane. An electrochemical gradient is created when these hydrogen ions stack up on one side of the membrane. The electrochemical gradient is the force driving the production of ATP from ADP. Energy from food creates the electrochemical gradient, the electrochemical gradient drives the production of ATP, so, thusly, energy from food is converted into ATP.

etc.JPG

As the high-energy electrons are passed along down the inner mitochondrial membrane they occasionally break free. When they break free, they become free radicals. These rogue free radicals can then attack other molecules and damage them. Because these free radicals are loosed within the mitochondria, the closest molecules for them to attack are the fats in the mitochondrial membranes. If enough of these fats are damaged, the membrane ceases to work properly. If enough of the membrane doesnít work, the entire mitochodrium is compromised and ceases functioning. If enough mitochondria bite the dust, the cell doesnít work and undergoes apoptosis, a kind of cellular suicide. This chronic damage and loss of cells is the basic definition of aging.

So, if free radicals cause this damage, why canít we stop it with antioxidants? We do. But not the antioxidants that we take in supplement formĖthose donít make their way into the interior of the mitochondria where the damage takes place. Nature has endowed us with our own antioxidant system located within the mitochondria where, so to speak, the rubber meets the road in terms of free radical damage. The antioxidants produced require sulfur, which comes from the sulfur-containing amino acids, i.e. methionine. There are certain substances contained in particular foods that stimulate the enzymatic machinery that increases the production of these intramitochondrial antioxidants. Sulforaphane, for instance, a substance found in broccoli sprouts greatly stimulates a particular enzymatic pathway within the mitochondria, resulting in an increased production of antioxidants where they need to be. Sulforaphane has been shown to prevent cancer, vascular damage, and a host of other disorders thought to result from excess free radical damage.
Our defense against free radicals, then, really comes in two forms. First, the production of antioxidants within the mitochondria, and, second, by making the fats in the mitochondrial membrane less prone to damage. How can we do that? By making them more saturated.

Sulforaphane was identified in broccoli sprouts, which, of the cruciferous vegetables, have the highest concentration of sulforaphane.[1] It is also found in Brussels sprouts, cabbage, cauliflower, bok choy, kale, collards, Chinese broccoli, broccoli raab, kohlrabi, mustard, turnip, radish, arugula, and watercress.

Saturated fats arenít prone to free radical attackĖonly unsaturated fats can be damaged by free radicals. Fats that have double carbon-carbon bonds, i.e. unsaturated fats, are the only fats susceptible to free radical damage. If the fats in the mitochondrial membrane are more saturated, then the membrane is less prone to free radical damage.

(Saturated fats: cream, cheese, butter, and ghee; suet, tallow, lard, and fatty meats; as well as certain vegetable products such as coconut oil, cottonseed oil, palm kernel oil, chocolate, and many prepared foods.)

Do we know this will work or are we guessing? Weíre pretty sure this is the case for a couple of reasons. First, when animals are calorically restricted (so far the only sure-fire way to increase lifespan), their membranes become more saturated. It was first thought that caloric restriction would reduce the production of free radicals, but it turns out that it doesnít. Calorically-restricted animals keep firing off free radicals at about the same rate as their non-calorically-restricted mates, but the fats in their membranes become more saturated, presumably providing protection against assault by free radicals, allowing the animals to live longer. Second, we can graph the degree of saturation of membranes against longevity, and when we do, we find that animals that live longer have more saturated membranes. Take a bat, for example, compared to a mouse. Both weigh about the same, but the bat lives for about 20 years, the mouse for three or four. The batís membranes are much more highly saturated than are a mouseís.

How can we increase the saturation of our membranes? By eating more saturated fat. In papers Iíve read, authors have cautioned against this approach (not wanting to appear Ďnutritionally incorrectí of course), then have gone ahead and written about how they created a group of study animals with greater membrane saturation by feeding them more saturated fat.

Another way we can increase the saturation of the fats in the membrane is by keeping insulin levels low. There are enzymes in the cells that both increase the length of fatty acid chains (called elongase enzymes) and those that desaturate (called desaturase enzymes) the fats. The desaturase enzymes can make fats less saturated. Insulin appears to activate these enzymes, so chronically elevated insulin levels would tend to keep the fats in the membranes less saturated and more susceptible to free radical attack. I would venture that this is one of the reasons that hyperinsulinemia shortens life. One of the constant findings in studies of centenarians is a low level of fasting insulin, which would make sense given the ability of excess insulin to make the membranes more prone to free radical damage.

Many people seem to think that the cellular membranes wonít function well if they contain more saturated fat. They believe that a more rigid membrane creates problems for the proper operation of all the receptors and other large protein structures that reside in the membrane. They are right in a way, since a certain degree of fluidity is necessary, but where I think they are wrong is in their belief that the degree of rigidity or fluidity of the membrane is determined by the degree of saturation of the fats in the membrane. Itís determined by methylation, as was discussed in the previous post.

When you put the whole puzzle together, itís pretty easy to see why a whole-food low-carbohydrate diet works to maintain health and longevity.

It provides plenty of good quality saturated fat to help protect the cellular membranes from free radical attack. It provides plenty of methionine, which is both a source of sulfur for the antioxidants in the mitochondria and a source of methyl groups for methylation of the fats in the cellular membrane thereby keeping them more fluid while at the same time more saturated. And it keeps insulin levels low so that the fats are not desaturated more than necessary, once again keeping the membranes less prone to free radical damage.

(One other way that low-carb diets help with health and longevity is by keeping the cells de-junked. As we age junk proteins accumulate in the cells. Over time these junk proteins can compromise cellular function. The generation of ketone bodies, a common occurrence with low-carb diets, helps keeps the cells clean. See here for a previous post on the subject.)

I believe the first and most effective defense against free radical attack is a good diet. Second is moderate exercise. (The effects of exercise on free radicals could be another long post, but for now, take my word for it: exercise reduces the production of free radicals) Third is the addition of a few supplements. CoQ10 and lipoic acid both act as antioxidants, but more importantly, they serve to regenerate the bodies own antioxidants. And a good vitamin supplement without massive doses of specific antioxidants isnít a bad idea.

I take krill oil, fish oil, and curcumin daily without fail. I also take a vitamin E daily to stabilize the fats in the fish and krill oil. I take CoQ10 and lipoic acid several times per week. I take a multivitamin every now and then. And I take vitamin D3 in large doses throughout the winter. From time to time I take this or that other supplement depending upon whatís going on with my health, i.e. do I feel like Iím getting a cold?

Iím not a big fan of large doses of specific antioxidants because we werenít evolved to take them. Plants live in the sun and produce oxygen as their way of life. Both the sun and oxygen are harmful if not controlled. Plants have evolved a complicated antioxidant system to protect themselves from sun and oxygen damage. We consume these antioxidants when we consume plants. We get tiny amounts of a zillion different kinds of antioxidants, not massive amounts of single antioxidants. And we get all the raw materials for the production of our own antioxidants from meat. (This post has gone on long enough, so if you want to read more about my view on antioxidants, read Chapter 5 in the Protein Power LifePlan.)

In my view, this is how nature intended us to get our antioxidants, and, with the exceptions mentioned above, this is the way I intend to get mine.