Adrenal glands and adrenal fatigue: stress makes you a mess!


Everyone talks about the adrenal glands and adrenal fatigue. So guess what? I’m jumping on the bandwagon! Because I’m a copycat? No, because it’s a really important topic!

The adrenal glands are two glands that sit on top of the kidneys, and they have two parts, the cortex and the medulla. The adrenal cortex is the outer part and it produces important hormones like cortisol and aldosterone. Cortisol helps regulate metabolism and participates in the stress response, and aldosterone assists in controlling blood pressure. The adrenal medulla is the inner part of the gland and it produces hormones like adrenaline which also participates in the body’s response to stress. It is adrenaline that prepares your body to spring into action when stress arises. The adrenals don’t only function in response to stress however, they produce hormones that enable us to live. The hormones produced by the adrenal cortex are essential to life, while those produced by the medulla are not [1, 2].

Two main groups of hormones are produced by the adrenal cortex and these are glucocorticoids and mineralcorticoids. The hypothalamus and pituitary glands stimulate the release of glucocorticoids, while the kidneys stimulate the release of mineralcorticoids. Corticotrophin releasing hormone (CRH) is produced by the hypothalamus and it stimulates the release of adrenocorticotropic hormone (ACTH) from the pituitary gland. This signals the adrenals to secrete corticosteroid hormones. Hydrocortisone and corticosterone are glucocorticoids released by the adrenal cortex. Hydrocortisone is more commonly known as cortisol. Cortisol regulates metabolism (conversion of fats, proteins and carbohydrates to energy), and it also helps regulate blood pressure and cardiovascular function. Corticosterone works together with cortisol to regulate the immune response and suppress inflammation [1].

Aldosterone is the main mineralcorticoid and it helps the body maintain salt and water balance, and helps control blood pressure [1].

Sex hormones are also released by the adrenal cortex, but in small amounts, and their impact tends to be trumped by hormones like testosterone and estrogen which are released by the testes and ovaries respectively [1].

So clearly we can see the importance of the hormones secreted by the adrenal cortex and why they are necessary to support life.

The adrenal medulla hormones are released when the sympathetic nervous system is stimulated and this occurs in times of stress. This is where the fight or flight response comes into play. This process is initiated by the sympathetic nervous system when the body is presented with a stressful/threatening situation and the hormones produced by the adrenal medulla contribute to this response. Epinephrine and norepinephrine are the hormones here. Epinephrine is also known as adrenaline and when the body encounters stress, it is responsible for increasing heart rate and providing more blood to the muscles and brain. It also causes a spike in blood sugar as it plays a role in stimulating the conversion of glycogen to glucose [in the liver]. Norepinephrine is also known as noradrenaline and it helps epinephrine respond to stress. It can however lead to vasoconstriction with can lead to high blood pressure [1, 2].

Stress can be linked to a number of health issues including high blood pressure, heart disease and digestive problems for example. Stress leads to hormonal changes and changes in blood sugar, and it can cause the body to excrete nutrients and can adversely affect the immune system. The adrenal glands appear to respond to stress in stages. The first stage involves enlargement of the adrenals due to an increased blood flow to them. With continued stress the adrenals shrink, and beyond that, adrenal exhaustion sets in [2].

The stress response is meant to be transient however in our modern times this isn’t the case. Our overworked adrenals don’t get a chance to recover between bouts of stress, because there is frequently no ‘between’, so the overproduction of adrenal hormones persists. This can lead to a decrease in immune system function, decreased blood flow to the digestive tract (causing indigestion, and IBS), and an increase in blood clotting ability (leading to atherosclerotic plaque formation and heart disease) [2].

In terms of the stages, when someone with otherwise healthy adrenals is in the first stage they can function well as needed. With continued stress the body enters a resistance stage and this is where the adrenals become enlarged. Here too the person may be responding to and handling stress but they may also feel amped up and may have cold, clammy hands and a fast pulse, might have a decreased appetite but otherwise doesn’t have serious symptoms… yet. When in the exhaustion stage, the adrenals start to fail as they struggle to meet the demands placed on them. Symptoms of this stage include fatigue, digestive problems, obesity, depression, dizziness, fainting, allergies and other issues [2].

Those with overworked adrenals may crave coffee, sugar and salt. Sugar and caffeine stimulate the adrenals [2].

Have you heard of the HPA axis? It’s the hypothalamic-pituitary-adrenal axis. Corticotropin releasing factor (CRF) plays an important role in the stress response because it regulates the HPA axis. CRF initiates a cascade of events in response to stress that results in the release of glucocorticoids from the adrenal cortex, which lead to a number of different effects in the body. Feedback inhibition by glucocorticoids has an important role in the regulation of the magnitude and the duration of the release of glucocorticoids. The HPA axis is also regulated at the level of the hypothalamus, and the stress response is mediated in the brain stem by a variety of mechanisms [3].

When the stress response is activated, it initiates behavioral and physiological changes that provide an individual with a leg up if you will when it comes to survival in the face of challenges to homeostasis in the body. Behavioral changes include increased awareness, increased cognition, and even euphoria. Physiological changes include increases in cardiovascular tone, rate of respiration and intermediate metabolism. Other functions like digestion, growth, immunity and reproduction are inhibited. When stress persists, the stress response can result in pathogenic effects. For example, in order to maintain homeostatis in a state of stress, the body activates a range of responses that involve the endocrine, nervous and immune systems, and if the regulation of the stress response is inappropriate a number of conditions can develop including autoimmune disease, high blood pressure, affective disorders and even major depression [3]. The body was never meant to sustain the stress response, it is only there for us as a transient means for dealing with stress. And that my friends, it what all the fuss is about!

In addition to the information I’ve provided here, I was contacted by the author of a great book (and blog) that provides a ton of awesome detail on this subject. Check out The Adrenal Fatigue Solution!


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Homocysteine, say what?

I’m still on my ‘heart disease, it ain’t all about LDL’ kick. This time, it’s all about homocysetine! Homocysteine is a predictor of coronary, cerebral and peripheral vascular disease, and it is an intermediate amino acid that is formed during methionine metabolism. High levels of homocysteine in the body can be the result of deficiencies in vitamins B6, B12, and/or folic acid in that these vitamins are needed as cofactors for homocysteine metabolism. Increased levels of homocysteine appear to be responsible for the progression of atherosclerosis because of the endothelial (referring to the lining of the blood vessel walls) damage it may cause. It also promotes the deposition of LDL in the arteries [1].

All of the homocysteine in our bodies is made from methionine. Methionine is an essential amino acid that can be found in animal products. The fact that it is essential means you need to eat it to get it, your body can’t make it on its own. Vegetable sources are low in methionine, all of them, even protein veggie sources. I like to point that out because I am a meat eater and I think that animal products should be included as part of a well rounded and healthy diet (sorry vegetarians and vegans, just my opinion :)). There are two pathways by which homocysteine is metabolized, remethylation and transsulfuration. Vitamins B12 and folate are required for remethylation, and vitamin B6 is needed for transsulfuration [2, 3]. In the remethylation pathway, the enzyme MTHFR is involved, and this is where B12 and folate come into play (as cofactors for this enzyme). In the kidneys and liver another enzyme, BHMT plays a role. Enzymes involved in the transsulfuration process include CBS, and here B6 is the cofactor involved. In the transsulfuration pathway cysteine can be formed and is used in the synthesis of proteins and glutathione (the latter here of which is a very important endogenous antioxidant in the body) [2, 3]. 5-MTHF is the active form of folate and it works with B12 to donate methyl groups as homocysteine is converted to methionine. Usually about half of homocysteine is converted to methionine via remethylation, and the rest is transsulfurated to cysteine [2, 3]. Interestingly B2 (which is riboflavin), and magnesium are also required for the metabolism of homocysteine which points to the fact that a number of the B complex vitamins are needed for the maintenance of appropriate levels of homocysteine (which should be low), and to ensure it can be converted into compounds like glutathione [2].

Levels of homocysteine in the blood increase as we age, and particularly this increase begins in both sexes after puberty. While levels continue to increase with advancing age, concentrations tend to be lower in women than in men. Homocysteine levels are higher in the elderly and may be due to malabsorption of vitamin B12 or due to inadequate intake of B vitamins, impaired kidney function, or medications that interfere with vitamin absorption (like some antacids, H2 blockers and PPIs for example, think Pepcid, Prilosec and Nexium). Drugs like metformin (used to treat type 2 diabetes) can increase the breakdown of vitamin B12 and folic acid and therefore decrease their levels in the blood as well (potentially resulting in higher homocysteine levels). Smoking is associated with increased homocysteine levels, as is coffee consumption and alcoholism. Other lifestyle factors that may lead to increased levels of homocysteine include lack of physical activity, stress and obesity. There is also a genetic polymorphism that can result in increased levels of homocysteine, the MTHFR C677T polymorphism. One inherited copy of this gene can impair the body’s ability to methylate folic acid to 5-MTHF, and this is seen in about 40% of Hispanics and 35% of whites in the United States. If this gene is inherited from both parents, the individual will have a 20% higher risk of vascular disease [2, 3]. In terms of injury to the endothelium (lining of blood vessel walls), homocysteine can initiate the atherosclerotic process which leads to dysfunction of the endothelium, therefore leading to heart attack and stroke [2].

Back to methionine for a second, I can see vegans and vegetarians saying “oh yay, I don’t eat meat so my methionine will be low and therefore I won’t have a build up of homocysteine.” Not so fast my veggie friends! Methionine is a sulfur containing amino acid and it is important for things like the production of immune cells and proper function of nerves. Along with folic acid, in pregnancy, methionine plays a role in preventing neural tube defects like spina bifida in the fetus, it helps form glutathione, can prevent buildup of excess fat, helps with fatigue, and is good for your liver (rebuilding and repairing it). It may even be useful in treating Parkinson’s disease. BUT too much methionine can lead to more homocysteine so all of these good things are not reasons to take extra methionine. What you get from a well-rounded diet is exactly what you need [4]. Vegetarians and vegans however, you may want to discuss this subject with your doctor or nutritionist to make sure you are getting what you need in your diet!

You see folks, it ain’t all about the LDL!

  1. Pagana, K. D. (2010). Mosby’s manual of diagnostic and laboratory tests. Elsevier Health Sciences. P 301-302

Move over cholesterol, there are some new kids on the block


I’m continuing (if you’re following) my little series here on cardiovascular health. In terms of stressors to the vascular endothelium (the walls of your blood vessels), there are a number of things in the plasma that might be predictive of coronary heart disease (CHD) risk, and/or in assessing best treatment strategies for CHD. And I’m not talking about cholesterol! That’s right, there are other factors at play that may even be more predictive of your cardiovascular health than cholesterol!

In the plasma biomarkers like C reactive protein, homocysteine and lipoprotein(a) are of interest. The interest in these markers as risk factors for CHD are important because many folks that do have CHD do not have overt hyperlipidemia (high levels of blood lipids like LDL, and triglycerides for example) [1].

C reactive protein (CRP) is a marker of inflammation which is known to be part of the process in the development of atherosclerosis and thrombosis (clot formation). CRP is an independent predictor of risk for heart attack, stroke, peripheral vascular disease and sudden cardiac death even in those that appear to be healthy. Testing for CRP can provide general information that indicates inflammation exists in the body, but it’s not specific so it can’t tell you where that inflammation is. A high sensitivity C reactive protein (hs-CRP) assay is the test used to determine risk for CHD, but it’s not known if CRP is a sign of CHD or if it has a role in causing CHD. Inflammation in the body however can also be due to cancer, infection, IBD, and rheumatoid arthritis for example [1, 2].

Homocysteine is an amino acid and increased levels of it in the plasma is associated with aggregation of platelets, dysfunction of the endothelial cells lining the walls of blood vessels, inflammation and oxidation of LDL cholesterol. All of these factors can increase CHD risk. Measuring levels of homocysteine may be useful in those with known CHD that do not present with traditional risk factors (like smoking, hypertension, low HDL, and family history of CHD). I thought it was worth mentioning here that increased homocysteine levels may be present in those with low intake of folic acid and B12. What are good sources of these B vitamins? Folate can be found in mushrooms, green veggies, legumes, LIVER (yum!), and many grain products are fortified but that’s processed junk so not an ideal nutrient source. Vitamin B12 is found in animal products (sorry vegans and vegetarians) [1, 3, 4].

Lipoprotein(a) is lipoprotein small “a” and it’s also a biomarker of CHD risk in that it appears that those with elevated levels have an increased risk for heart attack and angina pectoris. It is rich in cholesterol and differs from LDL because it contains an additional protein (apolipoprotein (a)) [1, 5].

So there you have it. I will note that studies show that decreasing levels of these biomarkers of cardiovascular disease risk may not [yet] prove to lower such risk, but they do point to increased risk. See, there is way more to the story than just plain old cholesterol!

  1. Lee, R. D.; Nieman, D. C. (2013). Nutritional assessment. New York, N.Y: McGraw Hill. pp. 260-261

Size does matter: LDL particle size (and number)


So it turns out that the answer to the age old question “Does size matter?” is YES!

Lipids like cholesterol and triglycerides need to be transported from where they are absorbed or made to where they can be stored or metabolized. These lipids are fat soluble so they are transported by lipoproteins. The main lipoproteins that function as transporters are chylomicrons, very low density lipoproteins (VLDL), low density lipoprotein (LDL), and high density lipoprotein (HDL). These macromolecular complexes are known as apoproteins and they are involved in controlling interactions and the metabolic fate of lipoproteins. In terms of lipoprotein particles, there are three major ones, including HDL, LDL, and VLDL with HDL being the smallest and VLDL being the largest. In terms of composition, HDL is 30% phospholipid, 50% protein, 2% triglyceride, and 18% cholesterol. LDL particles are composed of 23% phospholipid, 25% protein, 9% triglyceride, and 43% cholesterol. VLDL particles contain 12% phospholipid, 13% protein, 60% triglyceride, and 15% cholesterol [1].

Chylomicrons are the largest of the lipoproteins and contain about 90% triglycerides. They are made in the intestines and carry dietary triglycerides from the small intestine to the liver, muscle and adipose tissue. They also carry cholesterol to the liver where the liver uses it to synthesize bile acids or can incorporate it into VLDL [1].

VLDL is made in the liver, and it can carry triglycerides to cells where it can be stored or metabolized. When VLDL loses its triglycerides it becomes IDL (intermediate density lipoprotein) which is smaller than VLDL, but larger than LDL. Some IDL is then transformed into LDL, and this links LDL production to the production of VLDL and the breakdown of IDL. LDL functions to carry cholesterol to body cells and is known as the most atherogenic of the lipoproteins [1].

HDL is the smallest lipoprotein and it is secreted by the liver and small intestines. Its role is the uptake of phospholipids and cholesterol from other lipoproteins and cells in the body. In terms of the risk for cardiovascular disease, I think most of us are aware at this stage that higher levels of HDL are associated with a decreased risk, while lower HDL levels are associated with an increased risk [1].

Regarding lipoprotein particle size, a decrease in plasma LDL particle size has been associated with coronary artery disease. There are four main LDL particle size groups that include large LDL, intermediate LDL, small LDL and very small LDL. This study notes that beta blocker use is associated with small LDL particles, and when use of medication was adjusted for in the cohort in this study, it was found that small LDL particles were still more prevalent in those with coronary artery disease when compared to the control subjects in the study. Both study groups had prevalent intermediate LDL particles. It was observed that the difference in LDL particle size in those with coronary artery disease and in the control population was significantly linked to high triglyceride levels and low HDL levels. Higher levels of HDL were observed in those with intermediate and small particles when compared to those with large or very small LDL particles [2].

In terms of measuring atherogenic lipoproteins, LDL particle number [and apolipoprotein B and lipoprotein(a)] can be useful in determining risk [of atherosclerosis]. LDL particle number measures the number of LDL particles, essentially the particle concentration, and this may be a stronger predictor for cardiovascular risk than LDL cholesterol levels. A low LDL particle number measurement is associated with a low risk for cardiovascular disease and appears to be more predictive of risk than LDL cholesterol measurements. This is because it’s possible to have low LDL cholesterol levels and high LDL particle numbers. So even with low LDL, you may be at risk [if LDL particle numbers are higher]. LDL cholesterol measures the amount of cholesterol mass inside the LDL particles making it indirectly reflective of the ability of the LDL particles to cause atherogenesis. In terms of particle size studies show that those with small and dense LDL particles have a much greater risk for coronary heart disease, whereas large LDL particles might provide a protective effect [3].

Bottom line here, there is way more to cholesterol than just your LDL, HDL and triglyceride numbers. New research has been emerging on this front, so next time you have your cholesterol checked, ask your doctor about LDL particle number and size! There are other markers of atherogenesis as well, so stay tuned, I’ll fill you in on those in upcoming posts!

  1. Lee, R. D.; Nieman, D. C. (2013). Nutritional assessment. New York, N.Y: McGraw Hill. pp. 258-259


Cholesterol and statins


Ever wonder how statins (cholesterol lowering drugs) work? Do you take statins and feel tired often, or do you take statins and feel you might be having cognitive issues?

Just about all the tissues in the body can make cholesterol. The liver makes about 20% of this cholesterol, and other tissues in the body make the rest (80%), and the intestines carry most of this responsibility. Cholesterol synthesis within the body (not from ingested sources) makes up more than two thirds of our daily cholesterol needs. There are a lot of different reactions that occur in the cholesterol synthesis pathway, however the process can be considered to occur in three stages. Stage one is the formation of HMG CoA, stage two converts HMG CoA to squalene (and this stage also includes the rate limiting steps of the process which is the reduction of HMG CoA to mevalonic acid by an important enzyme called HMG CoA reductase). In stage three, cholesterol is formed from squalene. Cholesterol is very important in the body. It is a component of cell membranes and it is used to make a bunch of different hormones, including your sex hormones (think testosterone in men and estrogen in women). When levels of total cholesterol in the body rise, cholesterol synthesis by the body slows down and this is the result of what’s called negative feedback regulation, and it occurs at the reaction that involves HMG CoA reductase (that’s stage two) [1].

Statin drugs function by inhibiting HMG-CoA reductase and therefore block the synthesis of cholesterol [1]. HMG-CoA reductase, as noted above, is involved in the rate limiting step in cholesterol synthesis. Statins also can decrease the availability of ubiquinone (coenzyme Q10 which is commonly known as CoQ10), and can impair the activity of cytochrome c oxidase which is an enzyme complex in the mitochondria (an organelle inside your cells that is responsible for making the energy you need to survive) and a maker of ATP (your body’s ‘gasoline’). Studies have shown that patients taking statins have decreased levels of CoQ10 and cytochrome c oxidase upon biopsy of their skeletal muscle. Nerve cells were also found to have decreased levels of both CoQ10 and cytochrome oxidase [2, 3].

CoQ10 functions in the body as an antioxidant and if not able to do its job, the result can be oxidation of mitochondrial DNA by free radicals. So when there isn’t enough CoQ10 (which can be associated with use of statins), mitochondrial damage and mutations can occur. In addition to this, statins also inhibit cytochrome c oxidase. Cytochrome c oxidase inhibition results in a lack of ATP production and this can lead to fatigue and weakness [2, 3].

Some studies even show that statins contribute to cognitive dysfunction. Other studies show they don’t [4, 5, 6, 7, 8].

Bottom line is that sure statins can lower cholesterol levels, but they do so by inhibiting a very important process in the body that is needed for energy production among other things. Is this good? NO! Should you stop taking your statins? NO! But it can never hurt to talk to your doctor, or better yet your nutritionist, for the full scoop! It might be possible, if you’re willing to do the work of course, to manage your cholesterol with diet and exercise. But don’t do it alone, talk to your healthcare provider.


  1. Gropper, S; Smith, J. (2013). Advanced Nutrition and Human Metabolism, Sixth Edition. Wadsworth. p. 92-96, 161, 172


Ketones and ketoacidosis, what’s the deal?


I hear often from those that fear low carb diets that one reason NOT to be on one is because ketosis might result, and therefore a risk for ketoacidosis. There is a big difference here between the body using ketones for fuel and ending up in a state of ketoacidosis (which can result in death). In dietary ketosis (which can be brought on by low carbohydrate diets for example) ketones flow from the liver to other tissues like the brain where they can be used as fuel. It is suggested that ketone metabolism and that mild ketosis may provide therapeutic benefits for a number of disease states like insulin resistance, and diseases that result from free radical damage (just think of all of the chronic diseases that are prevalent today if you are wondering which ones, like cardiovascular disease, diabetes, and cancer for example) [1]. Low carbohydrate diets also result in hormonal changes such as a decrease in levels of insulin and an increase in levels of glucagon, shifting metabolism in favor of gluconeogenesis (your body can make glucose which is a primary fuel source from other things that are not carbohydrates and this is a natural, healthy process). Even if no dietary carbohydrate is consumed (which is the primary source for glucose), it is estimated that 200 g glucose per day can be synthesized by the liver and kidney from dietary protein and fat [2]. In a fed state acetyl CoA formed in the liver during beta oxidation is oxidized to carbon dioxide and water in the Kreb’s cycle. This means that after eating, your body makes a substance (through a series of chemical reactions and a number of different intermediate products) that can then be used to make energy for the body. Beta oxidation is how your body does this by using fat as fuel. During times of low carbohydrate intake the rate of mobilization of fatty acids from adipose tissue increases and the liver can convert acetyl CoA to ketones (acetoacetate and 3-hydroxybutyrate). So when you don’t eat carbs your body takes the fat that it stores and breaks it down to produce energy, and ketones can result as this source of fuel. While the liver cannot use ketones because it does not have the enzymes needed to do so, ketones can replace most of the glucose (the typical fuel) required by the brain for fuel. During starvation or very low carbohydrate intake ketone bodies induce the blood brain barrier transporter for ketones to promote the flow of ketones into brain (in other words, your brain welcomes the ketones with open arms!). Continued use of some glucose by the body is necessary however (for red blood cells for example which can only use glucose) and is provided via gluconeogenesis [1, 2].

Diabetic ketoacidosis and dietary ketosis are very different ‘conditions’ and in severely uncontrolled diabetes if ketones are produced in massive quantities above normal they are associated with ketoacidosis. Specifically in type 1 diabetes the cells in the body are not able to use glucose that may be present in the blood because the insulin needed for this to occur isn’t available. This is why type 1 diabetics end up with high levels of glucose in their blood, and why they need to take insulin which can mediate the problem. Even though someone who is diabetic may eat carbs, if their diabetes is uncontrolled that glucose that results from carbohydrate metabolism can’t get into the cells (because of lack of insulin), the body will switch to using fat as fuel and therefore ketones can be produced. When this continues for sometime, it can become a life threatening complication of diabetes. The acids 3-hydroxybutyric acid and acetoacetic acid (these are the ketones) are produced quickly in this condition, and this causes a high concentration of protons (what makes these things acidic) to accumulate which overwhelms the acid base buffering system of the body (under normal physiologic conditions the body can easily keep from becoming too acidic, or too basic for that matter). It is this uncontrolled production of ketones and the overwhelming of the acid base buffer system that results in the condition known as ketoacidosis. Ketones produced when following a very low carbohydrate diet on the other hand are regulated and controlled, and the resulting dietary ketosis state is considered harmless, in that blood pH (acid base balance) remains buffered within normal limits [2].

Cool huh?

  1. (Links to an external site.)
  2. (Links to an external site.)

Image: https: //;_ylt=A0LEV7jOWgNVj34AUOIlnIlQ;_ylu=X3oDMTB0b2ZrZmU3BHNlYwNzYwRjb2xvA2JmMQR2dGlkA1lIUzAwMl8x?p=ketone&

I ‘C’ you


Vitamin C, what’s the hype? Vitamin C is also known as ascorbic acid and is a water soluble vitamin. Historically, vitamin C came into the limelight centuries ago because a deficiency of it results in scurvy. Many mammals can actually synthesize vitamin C on their own, BUT humans cannot (neither can fruit bats so I guess we are in good company, whatever a fruit bat is). The reason we can’t synthesize the vitamin is because we lack an enzyme (gluconolactone oxidase) needed in the pathway that synthesizes vitamin C. Vitamin C is actually a derivative of glucose (that sugar stuff our body uses for energy) [1, 2].

The best sources of vitamin C are fruits and vegetables however foods can be fortified which means vitamin C (in this case) is added in. Think breakfast cereals. Vitamin C is found in its ascorbic acid form in most foods however sometimes it is found in its oxidized form which is referred to as dehydroascorbic acid (it’s missing two protons and two electrons in this form). Vitamin C supplements come in several forms, including free ascorbic acid, calcium ascorbate, sodium ascorbate, and ascorbyl palmitate. Heat, light, oxidation for example, denature the vitamin, meaning deactivate it [1, 2].

Vitamin C is required for a number of bodily processes including the synthesis of collagen (a protein that supports important bodily structures like skin, bone, tendons, muscles and cartilage), carnitine (which is important for the body’s ability to use fats for energy), tyrosine (which is a precursor for the synthesis of neurotransmitters like norepinephrine and dopamine), and the synthesis of [other] neurotransmitters like serotonin. Our friend ‘C’ also is necessary for the synthesis of a number of different hormones like some of those involved in digestion. Vitamin C acts as a cofactor for enzymes that are involved in the biochemical reactions in the body play these roles. That means without vitamin C, these things wouldn’t happen because the enzymes needed to make these reactions occur wouldn’t be able to function! That makes vitamin C one important vitamin! Vitamin C also acts as an antioxidant. But hold onto your hats, vitamin C can also act as a pro oxidant, meaning it can promote harmful oxidation (and generate free radicals), BUT luckily that really hasn’t been proven to occur in the body, it seems to be the case in some science-y test tube experiments [1, 2, 3].

What about loading up on vitamin C to prevent getting sick? Well, since vitamin C is believed to play a role in the enhancement of the immune system it is believed, and has been widely studied, that the vitamin may help prevent and treat the common cold. While studies have not shown preventative effects of the vitamin on the common cold, it seems that regular use of it may reduce the duration of symptoms. Also large doses of vitamin C may reduce the duration of a cold, but it may only be useful if low levels of vitamin C are present to start with. Using supplemental vitamin C after the onset of a cold does not seem to be helpful. People with kidney disease should not take supplemental vitamin C, and taking more than 500mg at a time shows no advantage and the excess is either not absorbed or it is excreted in the urine [4, 5, 6].

It’s actually possible to consume too much vitamin C. Side effects that can result from vitamin C toxicity include stomach problems (abdominal pain and diarrhea), and people that have certain conditions that involve disordered iron metabolism should be cautious, as should people that have kidney problems in that excess of the vitamin can cause kidney stones. These last two cases of course are a smaller segment of the population [1].

Bottom line? Intake of vitamin C first of all should come from food sources, REAL FOOD sources like fruits and vegetables. Foods fortified with vitamin C are processed so definitely not ideal in any way shape or form for consumption at all [in my opinion] let alone to meet the required intake of the vitamin. And does it help when you’re sick? Maybe just a little!

  1. Gropper, S; Smith, J. (2013). Advanced Nutrition and Human Metabolism, Sixth Edition. Wadsworth. p. 307-318