NADH and anti-ageing - turn back time

Veröffentlicht am: August 01, 2024
Irina Fink
Irina Fink

Naturopath

NADH is also known as coenzyme 1 and is found in humans, animals and yeast. So basically it is part of every living organism.  

Research has confirmed that our NADH levels naturally decline as we age, which can lead to an increase in health problems. These include, for example, the development of chronic diseases, muscle loss and fatigue. 

However, some people also use NADH to treat high blood pressure, jet lag, depression, Parkinson's disease or to strengthen the immune system.

➤ Are you curious? Then read on to find out more about NADH.

Contents

What is NADH? 

NADH is the abbreviation for nicotinamide adenine dinucleotide. This substance is produced by our body from niacin, a B vitamin. 

But how exactly does NADH work in our body? 

NADH is known as a "helping molecule" because it binds to other enzymes and triggers reactions in the body that have a positive effect on our health. 

According to an article published in Scientific America, "a prominent theory of aging states that mitochondrial deterioration is a key factor in aging."

Mitochondria are specialized structures found in cells. They are involved in many cellular processes and, among other things, help to extract the energy stored in nutrients and convert it into a form of energy that can supply the body's cells with energy.

As mitochondria lose some of their power, this appears to contribute to diseases and symptoms associated with ageing. Examples include heart disease, cognitive decline and fatigue.

However, NADH is involved in energy metabolism and thus also in a number of bodily processes that make life possible. Some research suggests that NADH can restore and improve mitochondrial function. This not only increases energy levels, but also mental clarity, alertness, concentration and memory performance.

 

➤  Biohackers in particular like to use NADH. They speak of positive experiences in terms of endurance during workouts or running.

How is NADH produced by the body? 

There are a number of NADH precursors, such as amino acids and vitamin B3. Precursors are other substances that can be converted into NADH by the body, thereby increasing its levels. 

 

➤However, NADH is not always formed from amino acids.

 

In contrast to the essential nutrients that we can absorb from food, NADH is produced in the body from freely circulating amino acids. However, our body does not automatically synthesize these into NADH. Instead, the amino acids are broken down and used for various bodily functions.

We need niacin for our body to be able to produce the helpful molecule NADH. The vitamin known as B3 is found in abundance in meat, poultry, oily fish, peanuts, avocados, asparagus, broccoli, potatoes and liver.

This means that only if we supply our body with NADH in the form of food supplements can we be sure that its level will rise. 

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What effect does NADH have?

Proponents of NADH supplements believe that they can enhance the natural effects of NADH in the brain. 

 

➤ Some even go so far as to claim that it can restore memory and cognitive function in people with Alzheimer's disease. There is even ongoing research into whether NADH, administered by injection or intravenously, can slow the progression of Parkinson's disease.

We have summarized some of the convincing advantages and their background for you in more detail:

1. when energy levels drop - NADH as an aid for chronic fatigue syndrome

Most of the current research focuses on the use of NADH in the treatment of chronic fatigue syndrome (CFS).

➤  Experts believe that up to one million Americans are affected every year. Women are four times more likely than men to suffer from chronic fatigue syndrome. Women between the ages of 40 and 60 are particularly affected.

    • Studies have identified a possible correlation between low ATP levels and chronic fatigue syndrome. ATP stands for adenosine triphosphate and is a molecule that provides energy and is found in every living cell. Research suggests that NADH helps the enzymes in our body to convert food into energy in the form of ATP. This provides our body with more energy during the day.
    • In addition, NADH can reduce fatigue by restoring the function of the mitochondria. This releases more energy available for the body.
    • Research also shows that NADH can stimulate brain function. This improves memory, attention span and thinking ability, for example. This effect can alleviate the symptoms of chronic fatigue syndrome in particular, which is often associated with cognitive dysfunction. 
    • NADH can help your brain to produce neurotransmitters such as serotonin, noradrenaline and dopamine. They are all important substances in our brain that influence mood and cognitive function. This makes you feel more alert and, above all, happier. 

    A few studies have investigated the combined use of NADH and coenzyme Q10 in people with chronic fatigue syndrome. 

    • A 2015 study published in "Antioxidants and Redox Signalling" reported that in 73 women with CFS, the combined use of NADH and CoQ-10 led to an increase in physical and cognitive function compared to a placebo. 
    • The test subjects also reported more energy and an improved ability to concentrate. 
    • The results of the study also showed that the combination of NADH and Q10 is a true antioxidant package and protects our cells extremely well against oxidative stress.

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2. traveling again - combating jet lag with NADH

NASA investigated the effectiveness of using NADH as a countermeasure for jet lag. The reasoning was that NADH can stimulate dopamine synthesis and thus counteract the effects of jet lag in the form of cognitive dysfunction and drowsiness.

What did studies show?

  • 35 healthy frequent travelers were recruited for this double-blind, placebo-controlled study. The tests were carried out on the west coast before the test subjects flew overnight to the east coast.
  • The subjects received either 20 mg NADH or a placebo. All subjects were tested in the morning and afternoon of the day after the night flight to assess cognitive function, mood and sleepiness.
  • Jet lag led to drowsiness in half of the participants and to a deterioration in cognitive function in a third. In the morning after the flight, the test subjects showed attention deficits, impaired working memory, divided attention and visual perception speed.
  • Those who received NADH performed significantly better on cognitive and motor tests, performed better on other measures and reported less drowsiness than those who took a placebo.

NASA concluded that "stabilized NADH significantly reduced jetlag-induced cognitive impairment, was easy to administer, and had no adverse side effects."

3. fighting widespread illness - alleviating depression and anxiety with NADH

Anxiety and depression are complex disorders and there are several contributing factors. We know that the chemistry of the brain is altered by stress, anxiety, depression and other illnesses. 

Most antidepressant drugs act on the neurotransmitters in the brain. It is assumed that NADH works in a similar but natural way:

Crucially, NADH has a key role in the production of energy in our cells. When NADH levels in our cells are low, nutrients in the brain are depleted and we can experience anxiety, depression, sleep disorders and other mood swings. 

Increasing NADH levels has been shown to restore cellular energy, brain chemical levels and the right amount of neuroreceptors and neurotransmitters, bringing the brain back to its normal balance. This influences our mood and regulates the existing imbalance.

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4.getting there naturally - NADH as a supportive treatment option for Parkinson's disease

The coenzyme is particularly often associated with Parkinson's disease and touted as a promising treatment. 

The theory that NADH could affect Parkinson's disease (PD) was fueled by a 1996 study in which intravenous administration of NADH over eight days led to a temporary improvement in PD symptoms. 

Subsequent studies were unable to confirm these results. In some cases, the effects proved to be temporary and were therefore impractical. In others, no noticeable effect on PD symptoms was found. Nevertheless, research into the effect of NADH on Parkinson's is still ongoing. 

What side effects can occur when taking NADH? 

Experience has shown that NADH is very well tolerated and not harmful to our body, as it produces the substance itself. 

However, if used excessively, NADH can cause nervousness, anxiety and insomnia. When administered by injection, NADH can cause pain, swelling and redness at the injection site.

There is little research on the long-term safety of NADH. Although it is considered safe, NADH supplements should not be used in children, pregnant women or breastfeeding mothers.

Conclusion: 

  • NADH is also known as a "helping molecule" as it helps other enzymes in the body to manage a wide variety of processes and functions. It is found in every living organism. 
  • The molecule is said to improve mitochondrial function in old age. This is associated with increased energy levels and improved memory performance. 
  • Studies with different focuses suggest that NADH could be an effective treatment for chronic fatigue syndrome, jet lag, depression and Parkinson's disease.  

 

 

 

 

Sources (in English): 

Alraek, T., Lee, M.S., Choi, TY. et al. Complementary and alternative medicine for patients with chronic fatigue syndrome: A systematic review. BMC Complement Altern Med 11, 87 (2011). doi: 10.1186/1472-6882-11-87

Birkmayer, J. G., Vrecko, C., Volc, D., & Birkmayer, W. (1993). Nicotinamide adenine dinucleotide (NADH)--a new therapeutic approach to Parkinson's disease. Comparison of oral and parenteral application. Acta neurologica Scandinavica. Supplementum, 146, 32–35.

Gong, B., Pan, Y., Vempati, P., Zhao, W., Knable, L., Ho, L., Wang, J., Sastre, M., Ono, K., Sauve, A. A., & Pasinetti, G. M. (2013). Nicotinamide riboside restores cognition through an upregulation of proliferator-activated receptor-γ coactivator 1α regulated β-secretase 1 degradation and mitochondrial gene expression in Alzheimer's mouse models. Neurobiology of aging, 34(6), 1581–1588. doi: 10.1016/j.neurobiolaging.2012.12.005

Bushehri, N., Jarrell, S. T., Lieberman, S., Mirdamadi-Zonozi, N., Birkmayer, G., & Preuss, H. G. (1998). Oral reduced B-nicotinamide adenine dinucleotide (NADH) affects blood pressure, lipid peroxidation, and lipid profile in hypertensive rats (SHR). Geriatric nephrology and urology, 8(2), 95–100. doi: 10.1023/a:1008242900153 

Forsyth, L. M., Preuss, H. G., MacDowell, A. L., Chiazze, L., Jr, Birkmayer, G. D., & Bellanti, J. A. (1999). Therapeutic effects of oral NADH on the symptoms of patients with chronic fatigue syndrome. Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology, 82(2), 185–191. doi: 10.1016/S1081-1206(10)62595-1

Kuhn, W., Müller, T., Winkel, R., Danielczik, S., Gerstner, A., Häcker, R., Mattern, C., & Przuntek, H. (1996). Parenteral application of NADH in Parkinson's disease: clinical improvement partially due to stimulation of endogenous levodopa biosynthesis. Journal of neural transmission (Vienna, Austria : 1996), 103(10), 1187–1193. doi: 10.1007/BF01271203 

Rainer, M., Kraxberger, E., Haushofer, M., Mucke, H. A., & Jellinger, K. A. (2000). No evidence for cognitive improvement from oral nicotinamide adenine dinucleotide (NADH) in dementia. Journal of neural transmission (Vienna, Austria : 1996), 107(12), 1475–1481. doi: 10.1007/s007020070011 

Jesús Castro-Marrero, Mario D. Cordero, María José Segundo, Naia Sáez-Francàs, Natalia Calvo, Lourdes Román-Malo, Luisa Aliste, Tomás Fernández de Sevilla, and José Alegre. Antioxidants & Redox Signaling. Mar 2015.679-685. doi: 10.1089/ars.2014.6181

Swerdlow R. H. (1998). Is NADH effective in the treatment of Parkinson's disease?. Drugs & aging, 13(4), 263–268. doi: 10.2165/00002512-199813040-00002

Choi, W. S., Palmiter, R. D., & Xia, Z. (2011). Loss of mitochondrial complex I activity potentiates dopamine neuron death induced by microtubule dysfunction in a Parkinson's disease model. The Journal of cell biology, 192(5), 873–882. doi: 10.1083/jcb.201009132