Like most allopathic physicians, I have no formal training in herbal medicine. Nonetheless I tend to think that I have an open mind to non-Western therapies. I do not discount their effects in various conditions, but they are not the end-all-be-all of disease treatment and prevention, as some “health experts” would have you believe.
Unfortunately, terms such as natural or herbal have become synonymous with healthy and safe. Many people who tout the benefits of such products virtually always do so because they are concerned about the man-made (aka, non-natural) chemicals that allopathic medicine practitioners often prescribe, and believe (often without question) that natural treatments are better.
In allopathic medical schools, physicians are taught to critically analyze the scientific data that supports diagnosis and treatment. In current parlance, this is known as “evidence-based medicine.” I will certainly admit that much of what happens in medicine, in my own practice as well, is not fully backed by evidence, usually because not every detail of diagnosis and treatment has been rigorously tested, especially with more complex problems. Yet scientists, researchers, and clinicians involved in medicine try to find the answers and incorporate our experience with the scientific data, and when it does not exist or is uncertain, we need to use our best judgments.
This type of care is in stark contrast with the vast majority of natural therapy, which I will call CAM (for complementary and alternative medicine) from here on out for simplicity [even if there are other terms for CAM, I am using the blogger’s prerogative here]. CAM advocates who decry allopathic medicine usually tout their own wares based on experience and the report(s) of their patients or their mentors. This type of “proof” is the weakest type in science. A testimonial report of benefit is equivalent to a case report, whereas allopathic physicians depend on randomized, blinded, placebo-controlled trials to make our best decisions.
Few CAM therapies have actually been subjected to this type of scientific investigation, and when they are, most of the time they are no better than placebo. Although this is not universally true, it is one of the reasons that allopathic physicians maintain healthy dose of skepticism for CAM therapies.
I began this blog by saying that I have an open mind about CAM, and I really do. Most of the time therapies are generally safe. If they are safe but not markedly effective, the only real harm is to the pocketbook of the patient. Nonetheless, it is my responsibility to make sure I at least understand what the compound is, so I do what I can to look it up.
Recently someone asked me about a cough treatment, wild cherry bark, which her husband had purchased from a local organic store for his own cough. Knowing nothing about its composition or effects, I looked it up. Much to my surprise the active component is…HYDROGEN CYANIDE. Yes, the natural herb wild cherry bark consists of a poison.
Now its concentration in the herb may not be as high as it is in the pesticide or in the air of the gas chambers it’s used in, but I ask you…when did cyanide become safer and healthier than man-made chemicals that are tested in thousands of people before they are approved for distribution to the public?
Gut Check Blog 
Dr Madanick,
Your fears about cyanide in cherry bark cough syrup made me curious for more evidence about hydrogen cyanide. Here’s some from the International Programme on Chemical Safety. Your fears might be diminished by this information. Many foods contain it (table 3). Note that sodium nitroprusside, a medical therapy probably present in the UNC hospital pharmacy, is a hydrogen cyanide inducer in the blood of patients.
Table 3: Cyanide concentrations in food products.
Type of product
Cyanide concentration
(in mg/kg or mg/litre)
Cereal grains and their products
0.001–0.45
Soy protein products
0.07–0.3
Soybean hulls
1.24
Apricot pits, wet weight
89–2170
Home-made cherry juice from pitted fruits
5.1
Home-made cherry juice containing 100% crushed pits
23
Commercial fruit juices
Cherry
4.6
Apricot
2.2
Prune
1.9
Tropical foodstuffs
Cassava (bitter) / dried root cortex
2360
Cassava (bitter) / leaves
300
Cassava (bitter) / whole tubers
380
Cassava (sweet) / leaves
451
Cassava (sweet) / whole tubers
445
Gari flour (Nigeria)
10.6–22.1
Sorghum / whole immature plant
2400
Bamboo / immature shoot tip
7700
Lima beans from Java (coloured)
3000
Lima beans fom Puerto Rico (black)
2900
Lima beans from Burma (white)
2000
a From Nartey (1980); Honig et al. (1983); JECFA (1993); ATSDR (1997).
5.1.5 Other
Laetrile (another name for amygdalin derived from apricot kernels), which was formerly used as an anticancer agent, releases cyanide upon metabolism. Bitter almonds and apricot pits containing cyanogenic glycosides are still sold in health food stores and over the Internet (Suchard et al., 1998). Other drugs, such as sodium nitroprusside, which is used as an antihypertensive and in congestive heart failure (Guiha et al., 1974; Tinker, 1976; Aitken et al., 1977; Schultz, 1984; Rindone & Sloane 1992), also liberate hydrogen cyanide in the body. In sodium nitroprusside, the CN– moiety represents 44% by weight of the molecule. Some aliphatic nitriles that are widely used in the chemical industry — i.e., acetonitrile (IPCS, 1993), acrylonitrile (IARC, 1999), succinonitrile, and adiponitrile — also release cyanide upon metabolism (Willhite & Smith, 1981).
5.2 Human exposure
5.2.1 General population
The general population may be exposed to cyanide from ambient air, drinking-water, and food.
Based on an atmospheric hydrogen cyanide concentration of 190 ng/m3 and an average daily inhalation of 20 m3 air, the inhalation exposure of the general US non-urban, non-smoking population to hydrogen cyanide is estimated to be 3.8 µg/day (ATSDR, 1997).
Based on a daily drinking-water consumption of 2 litres for an adult, the daily intake of cyanogen chloride is estimated to be 0.9–1.6 µg (equivalent to 0.4–0.7 µg of cyanide) (ATSDR, 1997) for cyanogen chloride concentrations in water of 0.45–0.80 µg/litre (0.19–0.34 µg cyanide/litre).
Among the general population, subgroups with the highest potential for exposure to cyanide include active and passive smokers, individuals involved in large-scale processing of foods high in cyanogenic glycosides, individuals consuming foods high in cyanogenic glycosides, and, to a lesser degree, fire-related smoke inhalation victims.
Human exposure to cyanide by dietary intake is estimated to be potentially of major significance for cassava-consuming populations; cassava has been estimated to be the staple food for 500 million people. However, data on the concentrations of cyanides in the total diet are lacking; hence, the daily cyanide intake from food cannot be calculated. For human consumption, cassava can be eaten raw, cooked, or grated and roasted into flour and eaten as “gari,” which is the common form in Nigeria (Kendirim et al., 1995). In Mozambique, it was estimated that in families affected by the “mantakassa” disease (spastic paraparesis; see section 8), the daily intake of cyanogens was 14–30 mg (as cyanide) at the time of a mantakassa epidemic in 1981 (Ministry of Health, Mozambique, 1984b). In Nigeria, it was estimated that the intake of hydrogen cyanide in the tropical ataxia-endemic areas may be as high as 50 mg/day (Osuntokun, 1981).
Urinary excretion of thiocyanate has been applied in the biological monitoring of exposure to cyanogenic glycosides, especially among cassava-consuming populations. The average urinary thiocyanate concentration among children in the Bandundu region of the Democratic Republic of the Congo (formerly Zaire) was 757 µmol/litre in the south and 50 µmol/litre in the north (both populations consumed cassava as their staple diet, but the cassava was well processed in the north and inadequately processed in the south). These concentrations can be compared with an average of 31 µmol/litre in a non-smoking Swedish reference population (Banea-Mayambu et al., 2000). In the same Bandundu region, it was shown that there was a marked seasonal variation in urinary thiocyanate concentrations in the villages with a high “konzo” (spastic paraparesis) incidence (563–627 µmol/litre in the dry season and 344–381 in the wet season), while the average in non-konzo areas was 241 µmol/litre (Banea-Mayambu et al., 1997). In Mozambique, the average urinary thiocyanate levels among healthy children from areas with epidemic spastic paraparesis varied between 33 and 1175 µmol/litre, whereas levels in areas with no paraparesis were between 18 and 400 µmol/litre (Casadei et al., 1990). In Nampula province in Mozambique, where spastic paraparesis epidemics had been observed in 1981–1982 and during the civil war in 1992–1993, average urinary thiocyanate concentrations among schoolchildren in five areas were between 225 and 384 µmol/litre in October 1999 (Ernesto et al., 2002). In Malawi, in an area where cassava was typically soaked for 3–6 days for processing to flour, urinary thiocyanate concentrations were between 2 and 410 µmol/litre, with a median of 32 µmol/litre (Chiwona-Karltun et al., 2000).
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