Aldehydes and Candida Connection

Alright, so you have read somewhere that one reason that candida is bad for you is that it produces a certain aldehyde which is harmful to your health. This article will give you in-depth information on what aldehydes are, how they are connected to candida, how they affect us, what does scientific research say about these, what can you do about it and much more.

Aldehydes in our lives

Aldehydes are compounds naturally present in living systems.

Aldehydes are present in our food in small amounts. For example, benzaldehyde is the compound that gives bitter almonds their flavour, cinnamaldehyde is responsible for the typical flavour of cinnamon, and vanillin is the aldehyde from vanilla beans that gives vanilla its characteristic flavour.

Aldehydes are also present in essential oils and give them their anti-fungal, anti-inflammatory and calming therapeutic properties at high dilutions. If the concentration of aldehydes is high, then it can sometimes cause irritation and sensitivity due to the reactive nature of aldehydes – for example, cinnamon bark and lemon grass have higher percentage of aldehydes and a higher dilution of these must therefore be used.

Some aldehydes perform essential functions, for example, retinal is an aldehyde which combines with the protein opsin in the retina of eye and forms rhodopsin. Rhodopsin is the main compound involved in process of vision.

Aldehydes vary in smell – most of the smaller ones smell like rotten fruits while most of the larger ones are pleasant smelling and are used in perfumery. Others may have a not so pleasant smells, like butyraldehyde that smells of rancid butter.

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Formaldehyde is the simplest aldehyde and is formed in nature in the early stages of plant decomposition in soil. It is naturally present in foods and fruits in small amounts. It is a very reactive compound, is used in dyes, insecticides, as embalming fluid, and in some medicinal drugs.

And that brings us to acetaldehyde – one of the not so very nice aldehydes, especially when you are exposed to it in high amounts. Acetaldehyde is naturally present in fruits and foods, but can also be added as a flavour in foods. One of the ways that we ourselves produce acetaldehyde is when we drink alcohol – the alcohol is converted to acetaldehyde by our liver. It is this acetaldehyde that causes the symptoms of hangover. Other ways in which we get exposed to acetaldehyde is through the indoor climate (building materials, cooking, cleaning goods etc.), smoking tobacco and cannabis (which could be responsible for addiction), and plastic usage.

It is acetaldehyde which also has a connection with candida and is one of the sources of exposure to those with chronic candida infections. Although acetaldehyde is short-lived in our body and quickly gets broken down into acetate, it still has the ability to cause cell and tissue damage. Acetaldehyde causes mitochondria to not function properly and this in turn compromises the breakdown of acetaldehyde. Thus, as acetaldehyde accumulates the ability to break it down further it decreases causing a chronic cycle of accumulation and damage. Acetaldehyde can also react with other molecules like protein and enzymes and change their structure and function.

Harmful effects of acetaldehyde

Acetaldehyde is harmful to us in many different ways. As it is very reactive, it can harm us in several ways – it is toxic, is an irritant of skin and mucosa, causes damage to organs and tissues, and is also a possible carcinogen for humans. Some of the more systemic effects of acetaldehyde are:

Cardiovascular effects: A review article published in 2010 by Guo and Ren discusses how harmful acetaldehyde is to the heart. It causes enlargement of heart chambers (cardiac hypertrophy), disturbs contraction of heart, and is associated with abnormal heartbeat and blood pressure. Guo and Ren also discuss how acetaldehydes are involved in production of free radicals which indirectly decrease antioxidant defences of our body leading to oxidative damage. A 2010 review by de la Monte and colleagues from USA describes how malondialdehyde (MDA) which is formed by oxidation of fatty acids is itself a component of the atherosclerotic plaque (plaque build-up in the arteries), and can also modify LDL. Both MDA and acetaldehyde also react with various proteins and form complexes which release pro-inflammatory and adhesion molecules involved in causing atherosclerosis.

Liver damage: The review by de la Monte and colleagues also describes the effect of acetaldehyde on liver. One mechanism by which acetaldehyde causes liver injury is by forming complexes with liver proteins. Our body recognizes these complexes as foreign and produces antibodies against them. The antibodies then work against the liver damaging it. Additionally, the complexes that acetaldehyde makes with the cell-skeleton proteins cause derangement of liver cell structure and thereby liver function. Acetaldehyde complex accumulation also leads to scar tissue formation in the liver followed by liver fibrosis or cirrhosis. The atherosclerotic nature of acetaldehyde can also cause the blocking of the blood vessels important for blood supply to the liver thereby causing liver disease.

Blood cell and clotting mechanism dysfunction: The review by de la Monte and colleagues also describes the possibility that acetaldehyde can cause destruction of red blood cells (RBCs) by making complexes with proteins of the RBCs. Again, these complexes are considered foreign by our body and our body launches attack against them (and thus against the RBCs). Destruction of RBCs can cause anaemia and iron accumulation in the liver causing liver injury. An article from 1987 by Baraona and colleagues from USA showed that acetaldehyde can also be transferred by RBCs from liver to other tissues causing widespread damage. Furthermore, acetaldehyde inactivates several blood-clotting factors as reviewed in the article by de la Monte and colleagues.

Neurotoxicity: de la Monte and colleagues in a study published in 2011 showed some evidence that acetaldehyde can cause oxidative stress induced neuronal injury as was also shown by experiments carried out by the same group of researchers and presented at a meeting in 2007.

Vitamin deficiency: Acetaldehyde can also be a culprit behind causing certain nutritional deficiencies. In 1983, Takabe and Itokawa, researchers from Japan, showed in rabbits that vitamin B1 gets depleted when acetaldehyde is administered to them. In 2013, Catazaro and Brecher from USA published their research on the impact of B-complex vitamins on acetaldehyde based blood clotting dysfunction. They found that vitamins B1, B6 and B9 could reduce the effect of acetaldehyde on blood clotting dysfunction. This is because these vitamins react with acetaldehyde and form a complex. Thus, it follows that if there is acetaldehyde in the system, it will bind very easily to free vitamins and the vitamins will not be available to perform their own function leading to vitamin deficiency. Vitamin B1 is very essential for nerve function and neurotransmission. Chronic B1 deficiency (which occurs in alcoholics and is related to acetaldehyde) can produce psychological symptoms and reduction in short term memory.

Folic acid deficiency has also been linked to acetaldehyde mediated oxidation damage. Way back in 1989 Shaw and colleagues from USA demonstrated that folate is destroyed by acetaldehyde in this manner. Folate deficiency can also result in neuropathy apart from other effects.

Other effects: There are many other harmful effects of acetaldehyde also discussed in the review by de la Monte and colleagues – induction of cell-suicide, behavioural and physiological effects like memory impairment and sleepiness, and promotion of cancer in people dependent on alcohol.

Considering that acetaldehyde is so harmful to us, it becomes imperative for patients with candida infection to know more about a possible relationship of candida with acetaldehyde and what can be done to avoid issues with acetaldehyde.

Acetaldehyde and candida – is there really a connection?

Back in 1984, Truss came up with a hypothesis and indirect evidence that candida could ferment sugars to acetaldehyde. He carried out metabolic studies on 24 patients with chronic candidiasis and tried to correlate the symptoms with toxic effects of acetaldehyde. The interesting part about his hypothesis is that it can correlate these two and perhaps also provides a chemical link between yeast fermentation and metabolic abnormalities in patients with yeast susceptibility. Truss did mention that direct evidence will be needed to prove this hypothesis.

However, looking at literature since 1984, one cannot find any detailed studies on this connection. This lack of scientific evidence does not mean that there is no substance to the hypothesis, but that this line of thought has not been followed up rigorously by the scientific community. One of the reasons could be that chronic gastrointestinal overgrowth of candida is not widely accepted by the mainstream medical community.

New evidence, however, is coming up from scientific work that does point towards existence of this condition. For instance, a 2012 research by Gong and colleagues from China found a particular strain of Candida albicans in 60% of the 111 patients they tested for indigestion but only in 14.8% of 162 healthy individuals tested. Rao and colleagues in 2013 and 2014 showed that impaired movement and contraction of digestive organs and overuse of a certain type of antacids (proton pump inhibitor) are risk factors for fungal overgrowth in small intestine and that fungal overgrowth (including candida) can cause chronic gastrointestinal symptoms.

Well then, you would ask, is there any scientific evidence of candida producing acetaldehyde in conditions other than gastrointestinal overgrowth of candida?

In 1999, a report published by Finnish scientists, Tillonen and colleagues studied salivas of 55 people based on salivary acetaldehyde produced from ethanol. They divided the people into high acetaldehyde-producing and low acetaldehyde-producing groups. They found that 78% of high acetaldehyde-producing salivas had yeast colonization as compared to only 47% of low acetaldehyde-producing salivas. They then isolated candida albicans from these salivas and checked for their acetaldehyde producing ability by adding ethanol to their growth medium. They interestingly found that the candida from high acetaldehyde producing salivas produced significantly more acetaldehyde as compared to candida from low acetaldehyde producing salivas. This clearly showed that some strains of Candida albicans can produce more acetaldehyde from ethanol than others.

In 2008, Rautemaa and colleagues, also from Finland, published results of similar experiments with Candida albicans strains isolated from Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) patients. APECED is a genetic disease where there is autoimmunity to various tissues accompanied with candidiasis. Many of those suffering from this disease also get oral cancer. The researchers could show that Candida albicans from these patients produced large amounts of acetaldehyde in presence of glucose (at a concentration found in foods and drinks and the concentration which has also been found to increase candida biofilm formation and adhesion in mouth), but not in non-patient controls. Interestingly, all Candida albicans strains isolated from the patients as well as non-patient controls were able to produce high amounts of acetaldehyde from alcohol (at a concentration that can be found in mouth after social drinking or in other fermented products).

Rautemaa and colleagues also published an article in 2009 where they reported their studies on acetaldehyde production from ethanol and glucose by 30 candida species other than Candida albicans. They found in their experiments that while all candida isolates produced large amounts of acetaldehyde from ethanol, only Candida glabrata could produce acetaldehyde from glucose. They concluded that oral infection with candida species could lead to the production of acetaldehyde from both ethanol and glucose.

Thus, there is good evidence that candida species can produce acetaldehyde by feeding on alcohol or sugar. There is also clear indication that Candida glabrata which was earlier considered non-pathogenic is now found in many candida infections – especially in vaginal candida infections. It seems possible that infection with Candida glabrata could put you at a higher risk of getting acetaldehyde poisoning as this candida can utilize sugar to form acetaldehyde.

The interesting thing is that a 2006 study by Ehrstrom and colleagues from Sweden showed that there is no difference in the levels of glucose in vaginal secretions in patients suffering from recurrent vaginal candidiasis and women without any candidiasis. So it cannot be the glucose in the vagina that can be used by candida to form acetaldehyde. Donders and colleagues from Belgium had showed in 2002 that women who had recurrent vaginal candida infections also had impaired glucose tolerance (higher levels of glucose in blood than normal) without being diabetic. It is a possibility that women with vaginal candida infections may get the infection from the bowels due to close proximity of vagina and anus. Thus, a lower glucose tolerance combined with vaginal candidiasis could indicate presence of pathogenic candida (and possibly Candida glabrata) in the gut.So what has impaired glucose tolerance got to do with acetaldehyde? Well, everything. Low glucose tolerance means high glucose in blood – and high glucose in blood would mean candida in the gut has more glucose available to convert to acetaldehyde.

Now, very interestingly, in 1981, TIengo and colleagues from Italy had showed in rats that acetaldehyde inhibited insulin which was produced in response to glucose in the blood. The question is whether the glucose intolerance seen in women with candida infections is actually an effect of suppression of glucose-induced insulin by acetaldehyde produced by candida? In that case it is likely that infections with glucose utilizing candida are able to support their overgrowth by producing acetaldehyde from glucose, the acetaldehyde in turn inhibits insulin which results in higher levels of glucose in blood and again candida can use more glucose to grow. More research is needed by the scientific community in this regard to say anything for sure. However, it does seem like a possibility that when a person has Candida infection, sugar and alcohol intake can actually lead to production of acetaldehyde (by candida in the gut), which can result in glucose intolerance which in turn can aggravate your candida issues.

So, yes, there does seem to be a correlation between candida and acetaldehyde. Candida infections may put you at a higher risk for acetaldehyde related toxicity.

So what can be done to avoid acetaldehyde issues?

What does science say?

A systematic review of double blind random controlled trial for prevention or treatment of hangovers (which are caused by acetaldehyde accumulation) was published in 2005 by Ernst and colleagues from UK and Netherlands. They analysed studies on natural agents like borage, artichoke, prickly pear and a yeast based preparation and conventional agents tropisteron, propranolol, tolfenamic acid and fructose or glucose. Although there were encouraging findings for borage, a yeast based preparation and tolfenamic acid, only one controlled study was available for each and also the sample size was small with unvalidated symptom scores. Overall, they actually found no compelling evidence that any of the interventions studied were any good for treating/preventing hangovers.

A 2011 article by Rautemaa and colleagues from Finland demonstrated in laboratory that the acetaldehyde produced by candida from ethanol was reduced by 84% by xylitol – a sugar alcohol used as a sweetener. Xylitol seems to do this is by suppressing the activity of the enzyme that converts ethanol to acetaldehyde. These results need to be confirmed with animal/human trials. Also, it is worth remembering that artificial sweeteners may be linked to glucose intolerance as was showed in 2014 by Elinav and colleagues from Israel. They found that the artificial sweeteners saccharin, sucralose and aspartame changed the gut microflora which caused glucose intolerance. Another study published in 2013 on xylitol was conducted by Japanese scientists Tamura, Hoshi and Hori which showed that xylitol affected the intestinal flora of mice. Thus, even though xylitol seems like and may also be proven in the future to be effective in reducing acetaldehyde produced by candida from ethanol, one should be wary of the side-effects of xylitol intake. This is especially relevant for people with candida infections as dysbiosis is already a problem for them and they would not want to make the problem worse – xylitol intake could actually result in worsening of candida infections.

Vitamins may have an effect on reducing the impact of acetaldehyde. Ren and colleagues from USA published an article in 2004 which showed that vitamin B1 supplementation can prevent cardiac dysfunction, protein damage and cell suicide of heart muscle cells caused by acetaldehyde. They showed that other vitamins of B group did not have this effect.

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What other sources on internet say?

You will find plenty of information on the internet regarding many different products that claim to be effective in clearing acetaldehyde from the blood and preventing the acetaldehyde related harmful effects, especially where it concerns candida. There is not much of scientific evidence about most of these agents.

One of these is, for example, molybdenum. It is true that molybdenum is required for the activity of aldehyde oxidase – a liver enzyme that can break down acetaldehyde to acetic acid and allow its removal from the body. However, genetic and nutritional deficiencies of molybdenum are very rare as molybdenum is found in most foods and molybdenum amount required is very small. Department of Health, UK suggests taking a varied and balanced diet should be able to give you all the molybdenum you need. Unless you have a serious genetic disorder, you are very unlikely to have molybdenum deficiency.

What is the logical thing then to do to prevent acetaldehyde build-up?

Do not drink, especially if you have candida infection: Even if you do not have candidiasis, acetaldehyde can be an issue if you drink heavily. Even if you do not drink heavily, but have the genes that do not allow you to metabolize and break down acetaldehyde fast enough, you are at a higher risk of acetaldehyde toxicity. Now if candida comes into the equation, it increases your risk as candida can very easily metabolize alcohol to acetaldehyde.

Take a well-balanced and varied diet: This will help you get all the minerals and vitamins needed to detoxify acetaldehyde.

Do not try to kill candida very fast: This will prevent accumulation of candida toxins by allowing the body to get rid of them as they are formed. If you kill candida very fast, it is going to overwhelm your liver which serves the cleaning and detoxifying function which will lead to acetaldehyde accumulation apart from other toxins.

Keep your liver healthy: Prevent liver disease, drink lemon juice which increasingly is being shown to have detoxifying activity, sleep well and enough – there is some evidence that sleep deprivation can cause disturbed liver function and liver injury.

Listen to your body: Finally, learn to listen to your body. Start with simple things like stop eating when you get a signal you are full (and not try to eat up every tasty morsel on the plate), go to bed when the body tells you it is bedtime (and not stay up late because your favourite TV serial is on), don’t take coffee or sugar to keep yourself awake during work hours – work on your nutrition and you will find that you do not feel less energetic during work hours, drink water – not just when you are extremely thirsty (when you are extremely thirsty, you are already dehydrating). Listening to your body’s signals will reduce your stress hormones and toxic accumulations.

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