Recently a study that was published in the prestigious Proceedings of the National Academy of Sciences (PNAS) discussed how B vitamins (specifically folic acid, B6 and B12) may be able to slow the development of Alzheimer’s disease, slowing the shrinkage of brain volume (Douaud et al. 2013). This is not the first study of its kind, but is one piece of the mounting pile of evidence that suggests that one of the biggest causative factors of Alzheimer’s is elevated homocysteine levels, and that controlling homocysteine may be a viable treatment. It all started over 15 years ago, with the observation
Since 1998, when the Nobel Prize in medicine was awarded for the work on nitric oxide (NO) as a signalling molecule that was responsible for dilation of the blood vessels, research in NO has accelerated rapidly.
In the mid 1990’s two independent research teams from University of London and the Karolinska Institute in Sweden found that NO could be generated from nitrates that were abundant in green leafy vegetables like spinach, lettuce, kale and especially beetroot. This requires the activation of the NOx 3,2,1 pathway to be fully operational. In effect, nitrates consumed in foods are reduced by oral bacteria into nitrites and then in the stomach into NO.
Since then, other research groups have joined the effort to uncover nitrate’s amazing ability to generate NO that is quicker and much more efficient than the previously known pathway via the amino acid l-arginine. Unlike, l-arginine which is only operational in conditions with good oxygen and is dependent on the proper functioning of a family of enzymes called nitric oxide synthases (NOS), nitrates offer an alternate pathway (albeit a backup) for the body to generate the versatile NO molecule quickly at low doses and in low oxygen conditions! The latter is an important factor especially during a number of pathologies where oxygen is a factor and there isn’t enough supply to the tissues. For example, people with asthma, emphysema, chronic pulmonary obstructive disease (COPD), heart disease, Raynaud’s disease as well as other diseases where the circulation is poor and of course for athletes. During an intense period of exertion, the tissues, particularly the muscles will be oxygen deprived, under such conditions l-arginine will convert into NO very poorly if at all. In fact, a recent publication shows that l-arginine does very little for an athlete. An athlete can quickly go into hypoxia or lack oxygen when there is an urgent need for NO to be generated. Nitrates can offer an easy solution to this predicament.
Numerous recent studies suggest that nitrates do indeed improve the exercising capabilities of an athlete! More specifically, human cycling and intense ergonomic studies show that a prior intake of nitrates will reduce oxygen cost meaning for the same amount of oxygen an athlete can work that much harder and that much longer. The mechanism behind this is thought to be due to improved mitochondrial efficiency as well as improved circulation with consequent improved nutrient availability.
To date there are seven human studies showing that nitrates impact health in a positive way including reducing blood pressure, preventing formation of thrombi (clots that can cause heart attack and/or stroke), improvement in blood vessel elasticity, neuro protection in cardiac arrest survivors and of course in exercise physiology. In addition, there is plenty of animal data that confirms raised NO levels via intake of nitrates will prevent heart damage, reduce angina, enhance immune function, reduce bacterial, viral and fungal diseases and have an anti-inflammatory effect. An intriguing application of nitrates might be in severely ill patients in the intensive care unit who are in a special predicament concerning the nitrate-nitrite-NO pathway for several reasons. The nutrition provided in the ICU is extremely low in nitrate (it’s pretty low in hospital food in general!) and due to sedation and intubation (a tube in the mouth), these patients have reduced production and swallowing of saliva. Many such patients are treated with a broad spectrum of antibiotics which can affect their oral nitrate being properly reduced by bacteria on the tongue. Moreover, these patients are often colonised with bacteria in their stomach which may be responsible for ventilator-associated pneumonia via regurgitation into the airways. Future clinical studies may reveal that gastric supplementation of nitrates/nitrites via intravenous drip may protect the gastric mucosa and prevent bacterial colonization.