Attention Deficit & Yeast Syndrome

If you are familiar with the books of William Crook, MD, then you are aware that “the yeast syndrome” has a strong connection to attention deficit. However, it isn’t only intestinal yeast or Candida that contribute to attention deficit. Intestinal bacteria are sometimes an even bigger factor.

Various substances produce by bacteria and yeast will affect your ability to think. For instance, some intestinal bacteria produce a lot of ammonia. Too much ammonia will increase the turnover of serotonin in the brain. Ammonia interferes with mitochondrial energy production. Ammonia will also increase GABA, an inhibitory neurotransmitter in the central nervous system, and this will change the way other neurotransmitters are used. Another example of a substance that will affect cognition is DHPPA. Clostridia bacteria produce DHPPA, a molecular mimic of norepinephrine and dopamine. Thus toxins from intestinal bacteria can affect your ability to think.

The bacteria and yeast in the gut will alter the immune system. The immune system can affect sleep, memory, learning and hormonal regulation. Eg. A toxin from bacteria in the gut called lipopolysaccharide (LPS) will increase an immune cytokine called IL-1. IL-1 is of particular concern in attention deficit because it can have a profound effect on memory and learning.

LPS can also cause central hypothyroidism. This type of hypothyroidism is not picked up by the usual blood tests. Hypothyroidism alters the way the brain uses neurohormones like serotonin, norephenephrine and epinephrine. Sometimes, merely correcting hypothyroidism with a thyroid hormone supplement will eliminate attention deficit. (With central hypothyroidism, it is particularly important to consider the use of natural thyroid and T3 thyroid hormone as opposed to the standard treatment of just T4 thyroid.)

Yet, please don’t start thyroid supplements while a child is still on Ritalin. The combined effect could be dangerous. Thyroid hormones increase the sensitivity of the body to adrenaline. When you first start taking thyroid hormones (especially ones that contain T3), there can be an initial period where this adrenaline sensitivity is very prominent. That is why Ritalin could be a problem. Ritalin augments the body’s sensitivity to noradrenaline. The combination could be additive and lead to things like a very rapid heart beat.

Fuad Lechin, MD, PhD has found two types of neurochemical disorders in attention deficit hyperactivity. One presents excessive free serotonin in the plasma, while the other shows excessive dopaminergic activity plus norepinephrine overactivity.

Free serotonin:

Free serotonin in the plasma can be caused by allergies, low magnesium, toxins from the gut, or free unsaturated fatty acids. (Stress, including low blood sugar, will release oils in their free fatty acid form.) To prevent the release of serotonin into the plasma, it may be wise to limit dietary polyunsaturated oils. Eg, Reduce intake of corn, safflower, soy, cottonseed, canola, peanut and even flax oil. (Some of the biggest sources of these oils are margarines, restaurant French fries, and pizza crusts.) If you want to reduce free serotonin, then adequate magnesium is important too. Magnesium stabilizes platelets and mast cells. This reduces their release of serotonin into the plasma. Eliminating allergies would also reduce the amount of serotonin found in the plasma. Glycine counters some of the effects of free serotonin. Glycine improves memory and learning, and is therefore another supplement worth considering. However, glycine can also make some bacteria and yeast healthy. You need to watch out for this if you decide to try a glycine supplement.

Excessive dopaminergic activity plus norepinephrine overactivity:

The Feingold diet will improve the liver’s ability to remove norepinephrine and dopamine. The Feingold diet reduces the strain on the liver’s sulfation pathway, which is used to remove norepinephrine and dopamine. This pathway is often weak in attention deficit. However, to truly heal, one needs to get to get closer to the source of the problem. There are reasons that this sulfation pathway can be weak. One possible culprit is mercury poisoning. Another is intestinal inflammation. Intestinal inflammation and mercury poisoning reduce the sulfates in the body. Candida/yeast also contribute to the sulfation pathway problem by loading the body with phenolics. Yeast create phenolics that need to be removed by the liver, often by this same sulfation pathway. Also, consider low thyroid function as a possible contributor to this condition. In hypothyroidism, there tends to be an excess of serotonin, epinephrine and norepinephrine. Thyroid also helps the liver work better.

references:

1.    Bamforth KJ, Jones AL, Roberts RC, Coughtrie MW, “Common food additives are potent inhibitors of human liver 17 alpha-ethinyloestradiol and dopamine sulphotransferases.” Biochem Pharmacol 1993 Nov 17;46(10):1713-20, also see the Feingold website.

2.    Lynch MA. “Interleukin-1 beta exerts a myriad of effects in the brain and in particular in the hippocampus: analysis of some of these actions.” Vitam Horm. 2002;64:185-219. Review

3.    Segman RH, Meltzer A, Gross-Tsur V, Kosov A, Frisch A, Inbar E, Darvasi A, Levy S, Goltser T, Weizman A, Galili-Weisstub E. “Preferential transmission of interleukin-1 receptor antagonist alleles in attention deficit hyperactivity disorder.” Mol Psychiatry. 2002;7(1):72-4.

4.    Lechin, Fuad, MD, PhD, has articles about neurohormones at his website. He is an emeritus professor at the Central University of Venezuela.

5.    Hauser P, Zametkin AJ, Martinez P,et al. Attention deficit-hyperactivity disorder in people with generalized resistance to thyroid hormone. NE JMed, 1993, 328:997-1001.

6.    West SA, Sax KW, Stanton SP, Keck PE Jr, McElroy SL, Strakowski SM, “Differences in thyroid function studies in acutely manic adolescents with and without attention deficit hyperactivity disorder (ADHD).” Psychopharmacol Bull 1996;32(1):63-6

7.    Wallace, D, “The Fibromyalgia Syndrome” Annals of Medicine 29:9-21,1997 and Brain Res 1999 Jan 9;815(2):337-48 and Wang J, Dunn AJ. “The role of interleukin-6 in the activation of the hypothalamo-pituitary-adrenocortical axis and brain indoleamines by endotoxin and interleukin-1 beta.”

8.    Schneider C, Delorme N, El Btaouri H, Hornebeck W, Haye B, Martiny L. “Interleukin 1 beta (IL-1 beta) action in porcine thyroid cells involves the ceramide signaling pathway. Cytokine 2001 Feb 7; 13(3):174-8 (Thyroiditis)

9.    Peat R, PhD, “Tryptophan, serotonin, and aging” Ray Peat’s Newsletter, January 2002 He explained that polyunsaturated free fatty acids could release serotonin from cells.

10.    Peat T, PhD “Autonomic systems” Ray Peat’s Newsletter, May 2003 “In hypothyroidism, it is common for there to be an excess of adrenalin/noradrenalin, serotonin, histamine, and some of the pituitary hormones.”

11.    Komisar J, Rivera J, Vega A, Tseng J, Effects of staphylococcal enterotoxin B on rodent mast cells” Infect Immun 1992 Jul;60(7):2969-75