1 - The Cholesterol Problem - Or Is It?
So, you have been paying some attention to the prevailing health warnings and advice regarding preventing heart attacks. Understandably so, since the combination of coronary arteries disease, heart attack and strokes add up to being the major cause of deaths in the world. You have been hearing for many years now that the plaques that are created inside our arteries resulting in their gradual narrowing, a process known as atherosclerosis, are made up by this fatty substance we all know as cholesterol. It would seem logical to assume that as long as you reduce the amount of fat in your diet, the cholesterol in your circulation will also be reduced and thus there will be lesser of it to be used as damaging, arterial narrowing material.
You will be surprised to hear however that several large studies involving thousands of individuals have concluded that low-fat diets just don’t work, or work long enough to permanently reduce cholesterol. They may lower it for the short term but with most people cholesterol after a while just climbs back up, returning to or often exceeding the original point, so that the real health advantages of dietary fats restrictions are close to insignificant.
You see, the vast majority of the cholesterol found in our arteries is manufactured by our liver, in fact some 80%, Only the other 20% actually is derived from our food |
Even if you stopped consuming all cholesterol-containing foods, your liver will simply increase its own manufacture, because cholesterol is critical for our life processes, you cannot live without it. A major constituent of our bodies, cholesterol is found in blood, brain tissue, the liver and the kidneys. It forms the walls or membranes of all our cells, our vitamin D and our key regulating hormones, progesterone, estrogen, testosterone and adrenaline.
Of greater importance than the total amount of cholesterol that our bodies manufacture are the mix of the two major types of cholesterol produced. Low-density lipoprotein (LDL) is the ‘bad’ cholesterol that becomes a threat to our arteries when it undergoes a molecular transformation called oxidisation.
High-density lipoprotein (HDL) is the ‘good’ cholesterol that transports the bad LDL cholesterol back to the liver for removal out of the bloodstream. For someone with heart concerns, a high level of HDL is one of the best readings to have. The higher the ratio of HDL to LDL, the better protected against developing fatty plaques in your arteries and thus avoiding heart disease you become. Your blood test results will indicate that your good cholesterol should ideally be one quarter of your total cholesterol If your total cholesterol is, for ease of calculation, say 6, than your good cholesterol to prevent plaque formation should ideally be a quarter of that i.e. a HDL level of 1.5. Even better if, and this is a figure that most of our patients will regularly achieve, the ratio is one-third, meaning a higher good cholesterol, HDL level of 2 out of a total cholesterol of 6.
World leading Mayo Clinic has stated and many doctors now agree that your HDL ratio is a more important indicator for predicting the risk of heart disease than your total cholesterol |
They recommend an optimal ratio of 3.5 meaning that with a total cholesterol of 6 ideally the HDL or good cholesterol should be 1.7. Essentially the higher the ratio (i.e. a quarter (HDL of 1.5), a fifth (HDL of 1.2) or a sixth (HDL of 1) etc., the higher the risk of heart disease.
So what is wrong with a low-fat diet? For many, a low-fat diet will often mean feeling hungry again, often shortly after a meal. This will probably cause them to consume greater overall amounts of carbohydrates. These, refined carbohydrates in particular, are, as we have discussed, capable of elevating our blood sugar levels too rapidly causing our pancreas to produce high levels of insulin. High levels of insulin promote the formation of damaging LDL cholesterol as well as causing weight gain and increasing levels of fatigue and tiredness.
The low-fat and low-cholesterol diets – and therefore by default high carbohydrates – aggressively promoted in the 70s and 80s are largely responsible for the metabolic syndromes, including diabetes and cardiovascular disease which afflict the world today |
Eating a healthier and more satisfying diet, avoiding refined carbohydrates and various stimulants and supplementing their diets with the right natural supplements to help improve the liver functions and reduce oxidisation has assisted many patients at our clinics improve their overall health.
It has also helped improve their physical and mental energy, overall wellbeing and reduce their bad cholesterol (LDL) while increasing their good cholesterol (HDL), therefore improving their cholesterol profiles and reducing their risk of cardiovascular problems dramatically.
2 - Triglycerides
Another very important blood test reading appearing together with your cholesterol results, whose importance is not emphasised nearly enough, sometimes until its levels have gone truly through the roof, are your triglycerides.
Science is not completely clear or how or why, but high triglycerides are frequently associated with not only poorly managed adult onset diabetes and pre-diabetes, but also form part of the group of metabolic disorders which we have been calling hypoglycaemia or metabolic syndrome. Elevated levels of triglycerides are also known to be a side effect of taking some commonly prescribed medications such beta blockers, diuretics, steroids and the birth control pill.
Studies show that it is very common for people with high triglycerides to have low levels of good cholesterol (HDL) and high levels of bad cholesterol (LDL) whilst also suffering with abnormal insulin levels. Therefore, science associates high blood triglycerides levels with a greater risk of the build up of fatty deposits in the arteries, and is thus regarded as independent risk factors for cardiovascular disease.
A recent study at Copenhagen Hospital University in Denmark concluded that high triglycerides represent a greater risk of stroke than high levels of cholesterol |
Combined high levels of triglycerides and the bad cholesterol (LDL) increase even more the risk of heart attacks and also some forms of cancer. The Australian Bureau of Statistics indicate that people with high levels of triglycerides had a 54.2% chance of having high levels of total cholesterol, 37.6% chance of higher levels the bad LDL cholesterol, 45.2% more likely to have low levels of good HDL cholesterol, twice as likely to have high blood pressure, and were three times more likely to be diabetic than those with normal levels.
Let us discuss a little more what these triglycerides are and what they do.
Our liver transforms the excessive sugars ingested during our meals or snacking, which the body’s cells do not require right now, into glycogen which is stored for later use by the liver as well as by our skeletal muscle.
However the liver and the muscle can only store a limited amount of glycogen and if there are more calories remaining from our meal than there is storage space available in the liver and the muscles, the glucose is transformed into triglycerides and with the help of insulin, stored away, mostly as fatty tissues in our bodies, often in places where we perhaps at times would rather not have them. You may think of triglycerides as efficient batteries, tucked away in our internal organs, hips, buttocks and bellies, for emergency use should the electricity ever get cut off for whatever reason.
So, if one consumes too many calories which the body cannot utilise, particularly easy calories such as carbohydrates and fats, as well as putting on unwanted fat, one could develop higher than desirable levels of triglycerides in one’s blood, hypertriglyceridemia.
When we are not eating, in between meals or worse at times of starvation or famine, our blood-sugar levels, as well as our insulin levels, drop and our blood adrenaline rises. The net effect of this causes the release of a fat dissolving enzyme, lipase, which starts the task of breaking down the triglycerides stored in our fatty tissues for release back in our blood where they first came from, to be utilised again as energy.
Triglycerides are substances that can perhaps be easily remembered as a chemical formula resembling the letter “E” in uppercase. The spine of the E shape resembling triglyceride consists of a glycerol molecule and the free legs are each a fatty acid.
Lipase breaks down the stored triglycerides in an orderly and progressive fashion ‘one leg’ (fatty acid) at the time, transforming it at first to look more like a letter F (or a diglyceride) and then a monoglyceride (kind of a number 7) and then finally a free glycerol spine, without any legs.
By virtue of this formation and breakdown of triglycerides process, twice as much energy can be supplied to our bodies than the energy that could have been directly by sugar alone.
The sugar stored in our muscles in the form of glycogen is reserved for usage by our muscles alone and, in times of fasting or starvation it will not be released or shared with any other organs in our body which are also, at the same time, starving for glucose, such as our brain. However, sugar stored in our liver also in the form of glycogen and which gets changed back into glucose when our blood glucose is low, can and will be released into our blood and shared for use as energy by any organs that require it.
The sugar storage capacity in our muscles and liver is rather limited and can be depleted in a single day. The energy stored in the form of triglycerides in our fat cells can provide us with energy for up to a whole month or more |
The three fatty acids that were being progressively released into our blood during the breakdown of our triglycerides, get absorbed from the blood into our body’s cells where they get further broken down for energy utilisation through a process called beta-oxidation. Some of these three fatty acids will also find their way to the liver, where they will also undergo further breaking down into energy generating by-products which include substances known as ketones. The brain, which as mentioned earlier is the major user of the glucose in our blood, can utilise these ketones in lieu of glucose. The remaining (legless) glycerol spine also finds its way into the liver for further breakdown into glucose.
Most blood tests will indicate that normal levels of triglycerides should be somewhere between 0.5 to 1.7 mmol/L in Australia (or 150 mg/dL in the US and some other countries) with 1.7 to 2.2 mmol/L being borderline high and above that either high or very high. It is not unusual for patients to come and see me for their first time at the clinic with recent doctor’s blood results on hand showing triglyceride levels of 4, 5 or sometimes even 6, who have not even been warned of their risks. To me even a level of 1.7 mmol/L is not ideal and, soon after our patients begin their treatment program, I aim for and usually get them down, in their next blood test, to at least one half of the 1.7 that is still considered normal. Ideal levels of 0.5 to 0.7 are quite commonly achieved by most of our patients. Contrary to the commonly long held medical belief, we achieve this not by going on an extremely low fat diet, which seldom works anyway, but by simply reducing the excessive carbohydrates, particularly junk food, and implementing a regular protein and good fats dietary program together with the appropriate natural supplements required to improve the liver, the cellular absorption of glucose and its inside of the cell processing into energy.
For these patients their cholesterol levels also improve with results commonly showing a higher levels of good HDL cholesterol and lower bad LDL cholesterol and therefore better HDL to total cholesterol ratios, commonly below 4 and often close to or below 3. The same process slowly reduces the high blood pressure, high insulin levels, normalises blood-sugar levels in diabetics and pre-diabetics, and patients receive the previously mentioned comments from their doctors “whatever you are doing is working so keep it up”.
But stabilizing hypoglycaemia or metabolic syndrome isn’t all just about diabetes, blood pressure, cholesterol or cardiovascular disease. As a matter of fact hypoglycaemia/metabolic syndrome can and usually does affect virtually everything that everyone almost always presents themselves for in my or any other health practitioner’s clinic, as we will discuss a little later on.
Insulin therefore plays an incredible role of beneficial importance when our diet is devoid of useless food, we lead reasonably active lives, our stress levels are under control and we are happily enjoying whatever life brings us, and it can virtually destroy our health and lead to an earlier demise when we don’t.
It is not just about insulin, it is always all about insulin |
3 - Homocysteine
Well, for those who thought that the last few pages on triglycerides were somewhat revealing, wait until you hear about the next problem that, particularly when piggybacking on the ones we have just discussed, can increase even more the chance of meeting the world’s biggest killers, cardiovascular disease, heart attack and stroke.
The problem is a substance in our blood called homocysteine. Most doctors know about it but many still avoid having their patients levels checked out at blood tests, sometimes even when their cholesterol, triglycerides, blood sugar and blood pressure readings are high, and clearly place the patient in a higher heart attack risk category. It is produced in a biochemical reaction that every cell in our body has to perform in order to be healthy, perform its tasks and survive. This reaction is called methylation.
Don’t worry if you don’t know much about methylation, most health professionals have only just began hearing about it too. It is a complex reaction but you do not need to know all about it. Few really do and most who claim they do only think so. You only need to know enough to know how high levels of homocysteine affect our bodies and how, if you suspect you could be affected, to get your doctor help you verify it and treat it.
Firstly, how do we get to develop high blood levels of homocysteine (hyperhomocyteinemia) and what problems can it cause?.
Homocysteine is a form of amino acid, that, unlike many of the metabolic problems discussed this far, is not usually brought into our bodies by what we ingest but it could be generated by what we fail to ingest, namely vitamins B6, B12 and folic acid. It could also be caused by genetic problems, which we will also discuss soon.
Higher than normal levels of homocysteine flowing through our arteries have been associated with atherosclerosis and thrombosis which may eventually narrow or block the arteries substantially, reducing the flow of blood and increasing the risk of heart attacks and strokes. Scientists have also noted a strong relationship between high levels of homocysteine in the blood and the narrowing of the carotid artery which brings needed blood to our brains and the presence of which increases another health problem which is also quickly moving towards epidemic proportions – Alzheimer’s disease and other types of dementia. Other risks include deep vein thrombosis (DVT) and the lodgement of thrombi into our lungs and thus pulmonary embolism, all serious and life threatening conditions.
Other more recent studies have found an association between high levels of blood homocysteine and shortened telomeres in the chromosomes of certain cells particularly leukocytes. Chromosomes are DNA molecules, the programs in the nucleus of the cell that carry all of our genetic information within each one of the trillions of cells that make who we are.
In order for us to be alive, cells need to reproduce and they do so by replication, one mother cell divides into two identical daughter cells. During the replication process each of the strands of chromosomes also duplicate, and are taken into each of the daughter cells with hopefully, the least amount of damage, so that the two photocopies are as close to the original photocopy as possible.
Telomeres are parts of our chromosomes, their tips to be more precise and they play a vital function to protect the chromosome from damage and fusion with other chromosomes when replicating. Telomeres, in their role of protecting the chromosomes, do become damaged and despite there being a regeneration of telomeres process within our bodies, telomeres shortening dysfunction is now recognised as an increased degenerative risk.
Recent studies have found strong evidence that the shortening of telomeres can be strongly influenced by our diets as well as by individual vitamins, particularly folic acid. Therefore, the shortage of folic acid or folate in our bodies is not only one of the possible factors responsible for greater level of homocysteine circulating in our blood and damaging our arteries but also with the faster degeneration of the telomeres placing our chromosomes at greater risk of damage during their replication.
The risks associated with damaged or shortened chromosomal telomeres have been widely investigated by science and include faster cellular aging, risk of cancer, Alzheimer’s and Parkinson diseases, rheumatoid arthritis, cardiovascular disease and more. An easier way to explain it is simply to say that the same process that causes high blood levels of homocysteine have been shown in many studies to also damage your telomeres and thus accelerates the ageing process and shortens lives.
Despite the high risk of illness, hospitalisation and mortality associated with high levels of homocysteine, modern medicine is still not recommending to check the blood levels of homocysteine in patients who “have a good diet with plenty of the B group vitamins in it”, unless the patient has actually already suffered a heart attack, stroke or a blood clot, or they have a family history of that disease. Unfortunately, many times this will have been too late.
Finding out after the heart attack or stroke that a simple blood test may have helped you prevent it is unlikely to bring much consolation |
Firstly, even the few people who are very particular about the quality of the food they ingest do not really know today how many vitamins and which vitamins are remaining in the commonly available foods which have been grown in soils depleted of minerals and vitamins, collected, stored transported processed and cooked in ways that almost always reduces the contents of health giving vitamins to at times extremely low and useless amounts.
Secondly, with the prevalence of low hydrochloric acid in many people’s stomachs as discussed in our earlier chapters, there is a strong risk of a further reduction in the absorption of what little vitamins are contained in our food. Particularly at risk is vitamin B12 due to intrinsic factor, also already discussed, Even if on paper our diet appears to be good, do we really know what we are absorbing and what we are not?
Thirdly, how often and when was the last time that your doctor thoroughly, or even not so thoroughly, questioned and discussed your diet to be able to determine whether you are likely to be absorbing and utilising your essential nutrients including vitamins B6, B12 and folate required to neutralise homocysteine and prevent the corresponding risks?
If he or she did, as I hope they will have, then they are probably a good, well informed doctor, and fortunately these days there are more and more around who dare to think outside the square and you should definitely stick with them.
The reason for their reluctance is because all medical and scientific observations of the effects of high blood homocysteine with coronary artery disease (CAD), heart attacks and strokes have not as yet been proven with absolute certainty, even though science accepts that high homocysteine is present in twice the number of people who suffer with these conditions than those who do not.
I guess tobacco companies also insisted for many prolonged years that because it could not be proven beyond the shadow of a doubt that smoking caused cancer even though smokers had a much higher rate of cancer than non-smokers, that therefore smoking was safe.
Whilst some may argue that the analogy may not completely apply to homocysteine, do you really want to wait for a few decades before science has more than just the current anecdotal evidence that the high homocysteine levels present in most cardiovascular disease victims is one of the major reasons for their condition?
I am sure that the smokers who had the vision of quitting smoking, even without seeing the smoking gun that proved that nicotine caused lung cancer, were very happy to have made the early choice of having done so. Particularly when the treatment for reducing high homocysteine problem does not have to be anywhere as challenging as giving up sugars or cigarettes.
4 – MTHFR
Let’s find about a little more how homocysteine is formed in our bodies.
Homocysteine is a naturally occurring amino formed in our bodies during a very important cellular biochemical reaction called methylation.
As stated earlier, the complete biochemistry of methylation can be very complex and I will therefore try to keep it within the practical context of this book by simplifying it and skipping large chunks of the full purpose and biochemistry of methylation.
To start with, let’s attempt to define methylation. Methylation is yet another very important function which occurs behind the scenes in our bodies and if it all goes well, we just take it for granted. After all who wants to spend time asking our bodies if they have methylated well today, nor congratulate our methylation process for contributing to us having had an enjoyable day full of vitality. However, we may certainly become very aware of its effects on our health and wellbeing should this process ever get out of balance.
The purpose of the methylation process is to add or more correctly transfer a molecule called a ‘methyl group’ to another substance, such as, for example, our DNA or a protein, so that the DNA or the protein receiving this methyl group may be able to perform whatever functions they are meant to perform.
As you can imagine both the DNA and proteins are the basis and the building blocks of life and are involved in a myriad of functions. Without methylation transferring the methyl group molecule in say our bone cells, they will develop problems in performing their function which is to produce healthy bone, hair cells for hair to grow, brain cells to perform a large number of different brain functions, etc., etc. It is during this methylation process that homocysteine, as well as other important molecules, is produced.
Probably the easiest way to visualise the methylation process is to think of a wall clock whose hour hands are going around and around.
The diagram below is a very simplified version of the methylation process to make it easier to explain the basic concept. For the readers who may become fascinated by this process and wish to get a more in-depth understanding, there is no shortage of information on the net together with far more detailed biochemical diagrams where the complexity is such as to make all the lines look like a bowl of spaghetti.
The methylation process begins at the 12 o’clock position on the above diagram, with an essential amino acid called methionine. Essential because the body is not capable of making its own methionine and should it not be in your food, then you will become short of it, with dire consequences for your health because of the many roles it plays. The best source of methionine are eggs, sesame seeds, cheese and brazil nuts but is also abundant in fish, meat and poultry.
Through a series of chemical reactions occurring between the 12 o’clock and 3 o’clock segments, methionine changes to s-adenisyl-methionine (SAM-e) at the 3 o’clock position in the diagram. The production of SAM-e is really the most important part of this cycle because it is SAM-e that donates or transfers the methyl group to the DNA, protein etc.
SAM-e then proceeds with a number of different reactions and changes and resurfaces at the 6 o’clock position on the diagram in the form of homocysteine.
Homocysteine, as you will have gathered by now, is really not desirable in our bodies in high quantities because of it being associated with a number of life risking and shortened biochemical activities. However, homocysteine is still essential, just not in high amounts, because driven by vitamin B6 it is capable of undergoing a series of changes which culminate through a process called transsulfuration with the production of glutathione, probably the most important and powerful antioxidant in our bodies. If homocysteine is too low, there may then not be enough of it to convert back to methionine at 12 o’clock and this could bring the cycle to a grinding halt.
So, homocysteine needs to undergo further reactions mainly driven by folinic acid, which is the activated form of folic acid, and vitamin B12 to transform it back to methionine, where it all started at the 12 o’clock position. The same cycle will then recommence, over and over again to keep on producing SAM-e for the purpose to keep transferring the methyl group.
The most common problem in this cycle is the lack of vitamins B6, B12 and folinic acid in the diet, causing a failure to break down homocysteine at the 9 o’clock position and change it back to methionine. When this occurs, homocysteine blood levels raise and associate themselves with the various health problems already discussed.
Some health care professionals had been aware for several decades that any patients coming to see them with high cholesterol, diabetes or cardiovascular problems and also high homocysteine required the lowering of this amino acid to lessen the patient’s risk of greater health problems.
I remember decades ago regularly telling my patients with high homocysteine that they had a very good chance of reducing it by supplementing with vitamins B6, B12 and folic acid, the most commonly available supplement form of the folinic acid. It would almost always work and work very well, but not always and occasionally, for reasons which only became obvious many years later, we could not reduce the homocysteine at all.
Well, one of the reasons for some people failing to reduce their homocysteine has become obvious to science in just the last few years and not too many health practitioners understand it nor believe in it as yet.
You see, methylation requires ‘folinic acid’. Most supplements contain ‘folic acid’. The names are almost identical but folic acid cannot play the role of folinic acid which is required at the 9 o’clock position in our diagram. However, we knew from our nutritional biochemistry education that we all had an enzyme in our bodies which could change folic acid to folinic acid. The enzyme has a long name of methylenetetrahydrofolate reductase or MTHFR for short.
It is only a relatively recent discovery that not everyone’s MTHFR enzymes are capable of changing folic acid into folinic acid, because of genetic errors |
These days many blood testing laboratories can do a blood test that lets you know the most common genetic defects that may render the gene in charge of encoding or causing the production of the MTHFR enzyme to be defective. Although there are more than 40 known MTHFR defects, there are two genes on our number one chromosome, one in position 677 and the other in position 1298 which have been studied the most and at the moment seem to carry the greatest health consequences. Unfortunately not many health professionals have even looked at this test for their patients as yet.
The genetic defects may affect the nucleotide encoding positions 677 only, 1298 only, or both. The defect may have been inherited from one parent only (heterozygous) or both (homozygous). If the blood test shows that there are no defects in either position, then we should be able to change folic acid into folinic acid without any real problems and allow homocysteine to break down into methionine.
If we only have a defect on say position 677 from one parent (heterozygous) our ability to change folic acid into folinic is estimated to be reduced by 40%, if homozygous then 70%. If 1298 is heterozygous there is a 20% loss of function and if homozygous a 40% loss. If both 677 and 1298 are heterozygous, then the term used is compound heterozygous with a 50% loss of function.
So far we have only discussed how genetic defects with our MTHFR enzyme can cause high levels of homocysteine in our blood. Unfortunately defective MTHFR enzymes can cause other repercussions within the methylation process, because if homocysteine does not change into methionine and the methionine levels from our diet also happen to be low because of other health stresses that confiscate even more of this already lacking amino acid, the SAM-e levels can also drop. SAM-e at 3 o’clock on the diagram is where the accomplishment of good methylation, the production of methyl groups, gets passed on to the many functions in the body which require this methyl group.
Case Study no. 17 – Pam’s personal testimonial. I met Bruno many years ago when suffering with extremely unstable blood-sugar levels. The levels read from extremely high to alarmingly and dangerously low. My GP was unable to help me, so on recommendation I contacted Bruno Marevich. He put me on a regime that brought me back from the brink of diabetes. His knowledge was far superior to others that I had spoken to and I am so very grateful for his help. Some months ago I, unfortunately contracted a nasty virus and eventually became ‘chronically fatigued’. I contacted Bruno and was overjoyed to find that I could see him soon for an appointment. Again, with his vast knowledge, encouragement and medication, I have gone from being bedridden to leading a normal life. Bruno Marevich is THE most knowledgeable and genuinely conscientious man (health provider/naturopath) I have ever known. I would turn to him before anyone else and have recommended him to many, many people. Pam S. |
COMMENTS: There was a time when Pam was so fatigued she could hardly get out of bed. We treated her digestive tract and blood-sugar metabolism and since then her health and energy have improved considerably. However, even though Pam is quite positive about her great improvements, she is still prone to episodes of fatigue and tiredness. In the last few years, with more laboratories beginning to test for MTHFR, I have asked Pam to have a blood test, which found Pam positive for compound heterozygous, a 50% loss of MTHFR function, casting more light on the reasons for her inability of living a completely fatigue free life up to now. As well as using activated B group vitamins these days we are also working at harmonising the many other biochemical reactions involved in methylation. Pam’s spirit is very determined to keep on working to get this unasked-for condition under control and is diligently following our current test trails to help us become more aware of her specific treatment and supplementation requirements. |
Also, folinic acid on its own, is not only required for methylation in the body but also serves many other important functions. The consequences of low SAM-e and low folinic acid can therefore amount to even more problems and more symptoms to challenge your health care provider, including depression, anxiety, tiredness, poor sleep patterns, poor red and white blood cell production, the “on and off” switching of inflammatory reactions, more rapid cellular ageing, poor detoxification of chemicals, impaired energy production, greater risk of neural tube disorders and spina bifida. People with this condition may also often develop eye problems, abnormal blood clotting, skeletal abnormalities, allergies, schizophrenia and other cognitive problems.
Wow, what a long list, but to complicate matters even further if possible the cells of untreated MTHFR defects sufferers will often not be able to deal properly with natural medication either such as herbs, minerals and vitamins. This makes them further prone to poor health and disease and presents the practitioner with many challenges requiring particular knowledge and experience of this condition in order to help the patient.
From a methylation cycle and a vitamins standpoint therefore you will be quite rightly beginning to suspect that the B complex group of vitamins plays a vital role in keeping this important process working particularly,B6 and B12. And,for not only those people with a genetic loss of function of their MTHFR enzyme but for everyone else too,also the activated form of folic acid i.e. folinic acid.
However, I hope that I have by now been able to also get some of the message across that our bodies are not simply an aggregate of many complex biochemical reactions, all of which can be fixed by just dropping-in the required drugs or missing biochemical ingredients where they are needed. Indeed this form of healing is very often the standard approach applied by many modern-day health care professionals.
Whilst not denying in any way that supplementing with specific vitamins and at times perhaps also drugs that target the specific problem or malfunction will often bring a level of relief and perhaps also some repair, true health and healing should be a process that enlists the cooperative assistance of the whole body. as well as our minds, and in particular our digestive tracts and blood glucose metabolism.
These two alone do not constitute our whole body but they are, in my opinion and in those of the tens of thousands of people I have helped at my clinics, the two main problems that this day and age are more likely to stop our bodies from being healthy.
Fix correctly your digestive tract and improve your sugar metabolism and your body will not fail to get itself back into a ‘healing mode’ |
This will either take care of your health problems or will at least improve the chances that whatever other work your body may require, whether they be medicines or supplements for the specific problem that is worrying you, will have a greater chance to work well for you.. A healthy body takes care of all of its problems better than one which is not.
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