I heard a phrase a few months ago: "It's not the alcohol that makes you fat, it's the food you eat after that does."
Many young people, especially girls, are the ones more likely to believe this. Many people opt to starve themselves during the day to allow a big alcohol binge later that night to avoid excess calorie consumption. I have already written an article entitled "Saving calories - why this doesn't work" and now again, will be illustrating why modifying your diet to allow for big party nights isn't going to work. The bottom line is, alcohol contains calories, and a lot of them. 1g of carbohydrate or protein contains 4 calories, 1 gram of fat contains 9 calories, 1g of alcohol contains 7 calories. Besides this fact, many alcoholic drinks are laden with sugar, which can rake up over 200 calories per drink.
In fact, new research from the UK Department of Health has shown the average wine drinker consumes an extra 2000 calories a month from alcohol alone which amounts to eating an extra 184 packets of crisps a year, or 12 whole days of normal eating per year. No wonder drinkers are piling on the weight. For men, the average beer drinker drinking just 5 beers a week, adds a shocking 22100 calories a year or 110 doughnuts a year to their nutrition food profile.
.
Despite all the calories consumed from alcohol, alcohol is directly linked to malnutrition. Although it can provide a substantial portion of our daily calorie requirements, it provides no nutrients, carbohydrates, proteins, fats, vitamins or minerals, but instead provides inflammation of several organs including the stomach, liver and pancreas while impairing our body's ability to absorb and digest proper food required to nourish it.
Doing exercise may prevent the damage we can see (weight gain), however exercise does not prevent the damage that we cannot see (liver damage, inflammation, toxic metabolite accumulation).
We all know the feelings associated with alcohol - our number 1 social mood enhancing drug and drink of choice. We know the up's and down's with a hangover often being a reminder of a good night before but an unpleasant suffering the next. We know on the basic level how it affects us, some worse than others, but do we really know what is happening inside our body?
Alcohol, blatantly put, is a toxic chemical that produces serious pathophysiological changes in the body that can lead to death overnight, or over a period of several years.
So what exactly happens when we drink alcohol?
Alcohol, known chemically as ethanol, is rapidly absorbed from the gastrointestinal tract. Because the body cannot store alcohol, it must process it, and get rid of it. This occurs by a series of detoxification reactions and follows the following metabolic pathway:
The liver is responsible for these oxidative reactions. The first step in alcohol metabolism is its conversion to acetaldehyde by the enzyme alcoholic dehydrogenase (ADH). In order to do this, we require nicotinamide adenine dinucleotide (NAD+) which during this reaction is converted to its reduced form NADH. This is where the toxicity really begins. Starting with:
Acetaldehyde is approximately 30 times more toxic than ethanol itself and is the major cause of alcohol-associated side effects. Acetaldehyde is normally converted to acetic acid (what we commonly call "vinegar") in another reaction as follows:
Acetaldehyde is converted by acetaldehyde dehydrogenase to acetic acid, again using NAD+ converting it to NADH. If there is an error in this conversion, severe toxicity can result from acetaldehyde accumulation. Some people have genetic mutations and weaknesses in these enzymes preventing their efficient detoxification mechanisms. This is especially common in Asians and American Indians, but is not very common in Caucasian subjects. People who do suffer from genetic mutations in these enzymes often have extreme nausea, vomitting and headaches associated with drinking alcohol as the body cannot detoxify the metabolites. This is one of the reasons some people can have 1 drink and suffer the effects as if they had drank 10 drinks. People who binge drink and consume a large amount of alcohol in a short space of time, whether or not they have genetic mutations, can cause a build up of acetaldehyde as AcDH is not able to cope with the high demand.
Acetaldehyde accumulation results in cross-linking reactions, where it can covalently bind to protein molecules forming protein adducts. Because enzymes are proteins, acetaldehyde can disrupt metabolism and other reactions in the body by disrupting enzyme function. Acetaldehyde has also been found to disrupt formation of microtubules in the liver, resulting in fibrosis. A good example for this is given by Steven Fowkes (http://www.ceri.com/alcohol.htm) who uses the example of cross-linking in leather tanning processes. Cross-linking agents are used to link flexible collagen proteins in the animal skin to produce a tough resistant type leather. In case you didn't know, acetaldehyde is used as a cross-linking agent in the manufacture of plastic.
This is why acetaldehyde from chronic alcohol intake causes cross-linking reactions in the human skin that cause it to age and become tough, inflexible and wrinkled. This is the reason why alcoholics have some of the toughest aged looking skin around. Cross-linking.
Even if acetaldehyde is metabolised, it gets converted to acetic acid which is broken down to acetyl CoA which can enter the TCA cycle to generate energy. In high concentrations, however, acetyl CoA is also the first molecule required in the metabolism of fat generating pathways. This is why in high amounts, alcohol is actually metabolised to fat, if all the energy generated cannot be used.
One of the reasons highly athletic people battle with alcohol even in small amounts is the fact that alcohol metabolism generates a lot of NADH. The problem here is that NADH is then used in reactions to convert pyruvate (an energy intermediate) into lactic acid by the following reaction:
This ends up causing lacticacidosis and build up of lactic acid in the muscles causes severe cramping and generally poor training capacity. Excess NADH fuels metabolism toward generation of lactic acid, and not the reverse. The reverse reaction to generate pyruvate could allow for the production of glucose by gluconeogenesis reactions. This is why alcohol consumption causes low blood sugar levels as no glucose can be synthesised in the body to counteract low blood sugar.
To combat this, the body draws on its glycogen stores to supply glucose to raise blood sugar levels. This is the the other major reason why athletes really feel the consequences the next day because athletes rely heavily on glycogen stores in the muscle tissue to provide power and energy. In this way, alcohol actually breaks down these precious glycogen stores by forcing the liver and muscle tissue to convert glycogen back into glucose, leaving the muscles feeling lethargic and fatigued and causing a serious impact on training ability.
As mentioned above, alcohol metabolism increases NADH, which in turn, increases the NADH/NAD ratio. As NADH accumulates, it slows down other enzyme activity of the TCA cycle, namely isocitrate dehydrogenase. This causes an accumulation of citrate and acetyl CoA, which is the first molecule required for fat synthesis. The high NADH/NAD ratio therefore directs metabolism away from energy production and rather fat generating pathways. These fats accumulate primarily in the organs involved in alcohol metabolism, which is why alcoholics often are found to suffer from fatty liver disease, fatty myocardium and fatty renal tubules. (S Gropper et al., Advanced Nutrition and Human Metabolism, 2009).
This fat may not always be visible to the eye, but under the microscope, the damage to our bodies is clearcut:
Heavy drinking causes alterations in metabolism leading to fat accumulation in the liver and looks like this:
Notice the fat as large white circular globules that accumulate in the liver tissue. This causes immense stress on the liver and eventually these liver cells start to die and are replaced by fibrous scar tissue. This starts the development of cirrhosis.
Cirrhosis is often a late complication of chronic alcohol consumption. Cirrhosis, in a nutshell, is the accumulation of extensive fibrous tissue in the liver as a result of inflammation caused by alcohol intake. Unfortunately, cirrhosis is not reversible and the prognosis for survival is poor. Directly quoted from my medical biochemistry textbook "The risk for cirrhosis in alcoholics increases dramatically in males who consume 80g/day and females who consume 20g/day for 10 years." Note that 80g is equivalent to 8 beers/glasses of wine a day, which means for females in particular, consuming only 2 glasses of wine a day for 10 years significantly increases your risk, because females have a smaller body size and in fact, fewer alcohol metabolizing enzymes in the system.
Induced Metabolic Tolerance
There is another way that alcohol can be metabolised in the body. This pathway is known as the microsomal ethanol oxidizing system (MEOs) which utilizes Cytochrome P450 enzyme CYP2E1 for the metabolism of alcohol. The enzymes in this system though, are what we call "inducible enzymes". These enzymes are inducible by ethanol, meaning that when ethanol is consumed in high concentrations, it can actually induce the synthesis of these same enzymes that degrade ethanol. Sounds complicated?
Basically what this means is that the more you drink, the more these enzymes are activated to produce more to deal with the heavy load, but in doing so, establish a state of metabolic tolerance. This is why the more you drink, the harder it becomes over time, to achieve the same drunk feeling and more alcohol is required to get drunk. However, the dangers here include the fact that when enzyme induction occurs, substances that are also metabolised by the same microsomal system also generate metabolic tolerance. This ultimately means besides becoming tolerant to alcohol, you will become tolerant to other substances metabolized in a similar manner too. These generally include medication, such as painkillers and anti-depressants which are often themselves toxic to the liver and kidneys and fuel addiction to these compounds.
Its not all bad news though!
Many studies have shown that in moderation, alcohol may have beneficial effects, particularly in the prevention of cardiovascular (heart) disease. Alcohol increases good (HDL) cholesterol which protects the arteries from hardening (atherosclerosis).
There are supplements one can take to lessen the effects of alcohol:
To help detox the liver and prevent hangovers:
Milk thistle
Vitamin B1
Vitamin C
The major detoxification reactions for dealing with acetaldehyde involve sulphur-containing antioxidants such as cysteine and glutathione as well as N-acetylcysteine (NAC). All of these can be purchased from local health stores. How these work is they contain sulfhydral groups in the molecule which bind to acetaldehyde to prevent it cross-linking. A typical dose is 200mg cysteine before and after consumption of alcohol with at least 500mg vitamin C (aim for 1000mg).
Other ways to prevent hangovers and low blood sugar, make sure you eat before you drink. Alternate your drinks with water and avoid drinking in rounds or you will likely end up drinking more than you initially anticipated.
Here is a very useful alcohol advice page including information on calories in drinks and units of alcohol:
www.drinkaware.co.uk
Enjoy in moderation, and drink responsibly. If you reached the end of this article I hope you learnt something new and something that opened your eyes.
Cheers!
Find me on Facebook on Nutrition through Science or Fitnessfacts100.
http://nutrins.blogspot.in
ReplyDeleteDifferences with hormones— Indeed, for some time, it was believed that the distinction between vitamins and hormones was no longer tenable. But there exists a fundamental difference between these two classes of active substances : the hormones are regulatory substances whereas the vitamins are accessory nutrients.
NADH is reduced and pyruvate is converted into lactic acid which dissociates into lactate at physiological pH which is mostly used as a metabolite(reconverted to pyruvate and into the citric acid cycle), while some is brought to the liver for gluconeogenesis. Much controversy revolves around the H+ produced and what happens to it but its pretty safe to say it is not the main contributor to acidosis in the context of exercise, I wonder if it is here but it is an interesting question.
ReplyDelete