Category Archives: Herbal medicines/supplements

Chilli Peppers for Heart Health and Pain

Substances found in chilli peppers called capsaicin and capsaicinoids have been shown to relax blood vessels in the heart to increase blood flow, reduce cholesterol and blood pressure.

The team found, for instance, that capsaicin and a close chemical relative boost heart health in two ways. They lower cholesterol levels by reducing accumulation of cholesterol in the body and increasing its breakdown and excretion in the feces. They also block action of a gene that makes arteries contract, restricting the flow of blood to the heart and other organs. The blocking action allows more blood to flow through blood vessels.

“We concluded that capsaicinoids were beneficial in improving a range of factors related to heart and blood vessel health,” said Chen, a professor of food and nutritional science at the Chinese University of Hong Kong.

Also see –

Thomas Martin LAc.

The Triage Theory and Supplementing For Healthy Aging

The importance of taking supplements along with a healthy diet, though at the very least a prudent healthy practice, continues to be controversial in mainstream medicine. Widespread deficiencies have been reported especially in the elderly, the poor, obese individuals, pregnant women and those undergoing sustained stress. The genetic need for micronutrients also likely varies greatly among individuals.

Dr. Ames who is emeritus professor of biochemistry and molecular biology at the University of California, developed the Triage Theory of optimal nutrition. The theory shows how over extended periods of time hidden deficiencies in vitamins, minerals and other micronutrients can result in age-related diseases.

When essential nutrients in the diet are limited the body shunts then into functions essential for immediate survival, such as reproduction, so on the surface an individual may appear healthy despite dietary deficiency. As we age however these hidden deficiencies begin to manifest in disease.

There are more or less 40 substances essential for every metabolic pathway in the body – approximately 15 vitamins that are co-enzymes and 15 minerals that are required in enzymes, two essential fatty acids, omega-3 and omega-6, and about eight essential amino acids.

Despite an abundance of macronutrients such as protein, fat and carbohydrates the modern diet is frequently deficient in many of the above micronutrients.

Such Triage Theory deficiencies are especially damaging to mitochondria, components in cells responsible for energy production. This age-related decay not only affects DNA/RNA but weakens cell membranes, reduces oxygen uptake, oxidises fats, increases the formation of cancer promoting metabolites. To this end Dr. Ames’ laboratory is currently working on the use of vitamins, minerals, antioxidants such as lipoic acid and the amino acid acetyl l carnitine to reduce cellular decline and degeneration.


From Dr. Ames’ website –

Inadequate intakes of vitamins and minerals from food can lead to DNA damage, mitochondrial decay, and other pathologies (7). Intakes below the…RDA, are widespread (e.g. in the U.S.: 56% for magnesium; 12% for zinc; 16% menstruating women for iron; 16% of women for folate) (7).

(Deficiencies) are particularly widespread among the poor, African-Americans, teenagers, the obese, and the elderly (7).

Inadequate intake of folate, B12, or B6 leads to uracil incorporation into DNA and chromosome breaks —a radiation mimic (8, 9).

Inadequate zinc in human cells in culture causes release of oxidants, oxidative damage to DNA, and inactivation of p53 and other zinc enzymes involved in DNA damage repair (10, 11).

Inadequate iron intake inactivates Complex IV in mitochondria, which causes oxidant release, mitochondrial decay, and DNA damage; in the brain complex IV inactivation mimics the neurodegeneration of aging (12, 13).

Biotin inadequacy from food is present in 40% of pregnant women; biotin deficiency in human cells in culture leads to oxidant release, DNA damage, accelerated mitochondrial decay, and premature senescence (14).

Magnesium deficiency in human cells in culture causes mtDNA- protein crosslinks, accelerated telemore shortening, and premature senescence (15).

I suggest evolutionary allocation of scarce micronutrients by enzyme triage is an explanation of why DNA damage is commonly found on micronutrient deficiency (7).

We are developing sensitive assays for measuring DNA damage in human blood (16) so as to determine what level of each micronutrient is optimum for keeping DNA damage to a minimum.

We are exploring the effect of high dose B vitamins in delaying the mitochondrial decay of aging (18)…An optimum intake of micronutrients and metabolites, which varies with age and genetics, should tune up metabolism and markedly increase health at little cost, particularly for the poor, obese, and elderly (7).


Also on Dr. Ames‘ research – Low micronutrient intake may accelerate the degenerative diseases of aging through allocation of scarce micronutrients by triage. –

Optimal micronutrients delay mitochondrial decay and age-associated diseases –  

Are vitamin and mineral deficiencies a major cancer risk? –


Harvard School of Public Health recommends a daily multivitamin supplement.

Here’s an example of a high-quality multivitamin supplement (add magnesium and calcium to complete it) –

Thomas Martin LAc.




Efficient Absorption Mechanism for Plant-source Iron Discovered

The following study outlining a new understanding of plant source iron absorption was reported in Science DailyE. C. Theil, H. Chen, C. Miranda, H. Janser, B. Elsenhans, M. T. Nunez, F. Pizarro, K. Schumann. Absorption of Iron from Ferritin Is Independent of Heme Iron and Ferrous Salts in Women and Rat Intestinal Segments. Journal of Nutrition, 2012; DOI:10.3945/jn.111.145854 –


 “Our study shows that this different mechanism of iron absorption from plant ferritin is more efficient and gives the intestinal cells more control. It can be a new way to help solve global iron deficiency,” says Dr. Theil…

…ferritin iron is absorbed in its protein-coated, iron mineral form by a different, independent mechanism; iron absorbed as ferritin, leaves the intestine more slowly, but may, provide greater safety to the intestines than iron supplements…

In addition to potentially being safer, causing less irritation to the intestines, absorption of iron as ferritin is easier for the intestine. The iron found in meat and non-meat iron supplements enters the intestine from food one iron atom at a time. Each entry step requires the intestinal cells to use up energy. When the intestine takes in a single molecule of ferritin, however, it gets a thousand atoms inside that one ferritin molecule, making iron absorption that much more efficient.

…the results demonstrate that ferritin-rich foods such as legumes can provide a significant source of dietary iron for those in the greatest need of increasing their iron consumption.

Legumes and other plant foods were found to be a good source of highly absorbable ferritin iron which seems to overcome the absorption inefficiency seen in those with iron deficiency. This is significant as it provides an environmentally sustainable supply of dietary iron in plant-based diets low or absent of animal foods. It also suggests that balanced, economically viable plant sources of iron in developing countries are realistically obtainable through agricultural reorganization and dietary planning.

One final point, countering the popular notion that vegetarian diets or diets absent in red meat promote iron deficiency is that the available evidence shows no difference between the incidence of  iron deficiency anemia in vegetarians compared with meat eaters. In other words both groups show a similar incidence.


Thomas Martin LAc.









Low Serotonin and Depression Link Questioned

An article in New Scientist magazine, July 24th, 2010 by Linda Geddes, reported on the research of Christopher Lowry of the University of Boulder, Colorado.

Though the theory has never been proven, it has generally been thought that depression results from low levels in the brain of the neurotransmitter, serotonin.

The article outlines the central discovery of Lowry’s work that high levels of serotonin in people with depression as well as multiple type of serotonin releasing neurons in the brain is prompting a reassessment of the treatment of depression by simply increasing the neurotransmitter using SSRI antidepressants.


Though not mentioned this rethink likely calls into question the use of Tryptophan in complimentary/alternative medicine to boost serotonin in order to treat depression and other disorders presumed to involve low serotonin.

The true picture appears more complex (which seems to be the way it goes in the evolution of medical theory – especially in popular approaches of natural medicine) where multiple types of serotonin neurons are likely to be regulated in independent ways.

Jerry Kennard of Health Central reports Lowry as thinking it

 far more likely that there are subgroups of serotonin neurons that are overactive during depression, rather than under-active as many people have assumed. The piecing together of evidence started over three years ago when researchers at the Baker Heart Institute in Australia discovered up to four times the normal level of serotonin in the brains of people panic disorder. In depressed people not receiving treatment it was two times higher. Another interesting finding was that long-term use of SSRIs in people with depression and panic disorder actually seems to decrease serotonin levels – although it isn’t clear why.       


In a PLOS Medicine essay,  Serotonin and Depression: A Disconnect between the Advertisements and the Scientific Literature, Jeffrey Lacasse and Jonathan Leo, cover the demise of the serotonin theory and the failure of the latest anti-depressant drugs to live up the media hype.

In subsequent years, there were numerous attempts to identify reproducible neurochemical alterations in the nervous systems of patients diagnosed with depression. For instance, researchers compared levels of serotonin metabolites in the cerebrospinal fluid of clinically depressed suicidal patients to controls, but the primary literature is mixed and plagued with methodological difficulties such as very small sample sizes and uncontrolled confounding variables…  Attempts were also made to induce depression by depleting serotonin levels, but these experiments reaped no consistent results [9]. Likewise, researchers found that huge increases in brain serotonin, arrived at by administering high-dose L-tryptophan, were ineffective at relieving depression [10].

Contemporary neuroscience research has failed to confirm any serotonergic lesion in any mental disorder, and has in fact provided significant counterevidence to the explanation of a simple neurotransmitter deficiency. Modern neuroscience has instead shown that the brain is vastly complex and poorly understood [11]. While neuroscience is a rapidly advancing field, to propose that researchers can objectively identify a “chemical imbalance” at the molecular level is not compatible with the extant science. In fact, there is no scientifically established ideal “chemical balance” of serotonin, let alone an identifiable pathological imbalance. To equate the impressive recent achievements of neuroscience with support for the serotonin hypothesis is a mistake.

With direct proof of serotonin deficiency in any mental disorder lacking, the claimed efficacy of SSRIs is often cited as indirect support for the serotonin hypothesis. Yet, this ex juvantibus line of reasoning (i.e., reasoning “backwards” to make assumptions about disease causation based on the response of the disease to a treatment) is logically problematic—the fact that aspirin cures headaches does not prove that headaches are due to low levels of aspirin in the brain. Serotonin researchers from the US National Institute of Mental Health Laboratory of Clinical Science clearly state, “[T]he demonstrated efficacy of selective serotonin reuptake inhibitors…cannot be used as primary evidence for serotonergic dysfunction in the pathophysiology of these disorders” [12].

Reasoning backwards, from SSRI efficacy to presumed serotonin deficiency, is thus highly contested. The validity of this reasoning becomes even more unlikely when one considers recent studies that even call into question the very efficacy of the SSRIs. Irving Kirsch and colleagues, using the Freedom of Information Act, gained access to all clinical trials of antidepressants submitted to the Food and Drug Administration (FDA) by the pharmaceutical companies for medication approval. When the published and unpublished trials were pooled, the placebo duplicated about 80% of the antidepressant response [13]; 57% of these pharmaceutical company–funded trials failed to show a statistically significant difference between antidepressant and inert placebo [14]. A recent Cochrane review suggests that these results are inflated as compared to trials that use an active placebo [15]. This modest efficacy and extremely high rate of placebo response are not seen in the treatment of well-studied imbalances such as insulin deficiency, and casts doubt on the serotonin hypothesis.

Also problematic for the serotonin hypothesis is the growing body of research comparing SSRIs to interventions that do not target serotonin specifically. For instance, a Cochrane systematic review found no major difference in efficacy between SSRIs and tricyclic antidepressants [16]. In addition, in randomized controlled trials, buproprion [17] and reboxetine [18] were just as effective as the SSRIs in the treatment of depression, yet neither affects serotonin to any significant degree. St. John’s Wort [19] and placebo [20] have outperformed SSRIs in recent randomized controlled trials. Exercise was found to be as effective as the SSRI sertraline in a randomized controlled trial [21].

Thomas Martin LAc.