As suggested in the last post growth hormone and its downstream partner IGF-1 have a somewhat controversial standing with regard to aging and longevity. Although observations of animals seem to suggest GH/IGF-1 shortens lifespan, such observations are not as clear with humans. Additionally, while GH/IGF-1 does seem to promote cancer it also to seems to prevent cardiovascular disease, depending on the context. Continue reading
The following post will be fairly speculative, so view it as a researched opinion piece. This post may have its inaccuracies and will evolve as I continue to research this topic. Herein I will be proposing some of my views on growth hormone and its downstream protein IGF-1 with particular respect to its role in aging and longevity. Continue reading
Given the evidence that high blood pressure can negatively effect heart disease risk, lowering blood pressure with diet is perhaps a reasonable goal. The following are my recommendations for lowering blood pressure with food.
1. Garlic seems to lower blood pressure (1). In fact, garlic seems to be one of the most effective anti-hypertensive foods studied on humans.
2. Hibiscus tea seems to powerfully reduce blood pressure (2,3) although it hasn’t been as thoroughly studied as the other items on this list.
3. Two minerals which appear to lower blood pressure somewhat are potassium (5) and magnesium (6). These minerals can be found in most fruits and vegetables. Calcium produces a fairly small reduction in blood pressure (7). Perhaps because it provides both calcium, potassium, and some magnesium dairy products appear to lower blood pressure to a decent degree (8). Fermented dairy, such as yogurt, may produce even greater reductions in blood pressure (9-11).
4. Although sodium is probably the first thing a lot of people think of when talking about diet and lowering blood pressure I think some caution is needed. I have a post upcoming on sodium, but essentially sodium may be worth lowering if a person has a large intake (10 grams a day, for example) but at a certain point sodium restriction may cause health problems. Some studies have suggested low sodium intakes may worsen insulin sensitivity and even shorten lifespan. I recommend roughly 1 to 1 & 1/2 teaspoon/ of salt per day, or about 2000 to 3000 mg of sodium for most people.
It seems as if many theories about nutrition take hold in popular culture as a function of our human tendency towards word association.
The old belief, held by many even today, that eating fat will lead a person to become fat is probably partly rooted in the words we use. However this belief is somewhat misguided (calories are the main dietary determinant of weight loss, not fat), so why did it catch on? Well, would so many people have clung fervently to the idea that a low-fat diet should be the go to for weight loss had we called the fat on our bodies “adipose tissue” as it is so often referred to in the medical field? What if we called the fat in our diet “lipids”, or some other interchangeable term? In an alternate universe following a different lexicon would there have been as many people following a low-lipid diet for the purpose of adipose tissue reduction?
Phrased like that I kind of doubt it.
A similar example can probably be noted in the widespread idea that sugar causes diabetes. Diabetes is a disease characterized by high blood sugar. Even though the sugar in this scenario is in fact glucose, the use of the word “sugar” has almost certainly established in the minds of people a connection between this “sugar” in the blood and your basic dietary sugar, made up of glucose and fructose.
Were our colloquialisms more accurate we would say diabetics have high blood glucose and call “sugar” either sucrose or a mixture of glucose and fructose, whichever was more appropriate in the situation. This may have alleviated some of the unscientific condemnation of “sugar” as a cause of diabetes and the inevitable recommendation that diabetics avoid sugar at all costs.
Clearly I am beginning this post with some critical pronouncements. However, this issue is, in my opinion, one of the most complex, misunderstood, and important topics in nutrition today. The vilification of fructose is an increasingly popular dogma which I strongly oppose not just because I disagree with it, but because of the ramifications of this belief. Some health “professionals” have gone so far as to make the obstructive claim that fruit is contraindicated in people with diabetes and a risky food in general given the fructose it contains.
In this post I will be evaluating the belief that “sugar causes diabetes” primarily by critically evaluating the claim that fructose adversely affects insulin sensitivity.
The relationship between acne and nutrition is not well determined. Although many theories abound regarding the role of things like chocolate, milk, fat, sugar, and numerous other food and food compounds on acne development none of these have actually been confirmed in controlled trials.
Perhaps this issue was best summarized by Apostolos Pappas in a recent review (1) of the scientific literature on diet and acne:
“We did not realize how daunting it would be to write an article dedicated to making sense of the relationship of acne to foods. It turns out that there are no meta-analyses, randomized controlled clinical studies, or well-designed scientific trials that follow evidence-based guidelines for providing solid proof…We reviewed the updated arguments, facts, and relevant data on this ancient debate, but we warn the truth-seekers among you that the jury is still out.”
However, one possible dietary factor is zinc. Several studies have investigated the ability of zinc to improve acne. A number of these studies reported some degree of benefit (2-7), although some reported no effect (8,9).
This treatment most likely works correct a zinc deficiency, so be aware that in the absence of a deficiency a high zinc intake, especially from supplements, may cause toxic effects such as nausea, tiredness, and copper deficiency as well as disregulated appetite and glucose control. The safest course of obtaining enough zinc in the absence of a medically diagnosed deficiency may be by increasing foods rich in it, such as red meat, shellfish and, to a lesser extent, white meats. Plant sources include many types of seeds, beans and lentils. However, these sources typically provide less absorbable zinc than from meat, so they may be less preferable in this regard.
1. Pappas A. The relationship of diet and acne: A review. Dermatoendocrinol. 2009 Sep;1(5):262-7.
2. Göransson K, Lidén S, Odsell L. Oral zinc in acne vulgaris: a clinical and methodological study. Acta Derm Venereol. 1978;58(5):443-8.
3. Hillström L, Pettersson L, Hellbe L, Kjellin A, Leczinsky CG, Nordwall C. Comparison of oral treatment with zinc sulphate and placebo in acne vulgaris. Br J Dermatol. 1977 Dec;97(6):681-4.
4. Verma KC, Saini AS, Dhamija SK. Oral zinc sulphate therapy in acne vulgaris: a double-blind trial. Acta Derm Venereol. 1980;60(4):337-40.
5. Michaëlsson G, Juhlin L, Vahlquist A. Effects of oral zinc and vitamin A in acne. Arch Dermatol. 1977 Jan;113(1):31-6.
6. Michaëlsson G, Juhlin L, Ljunghall K. A double-blind study of the effect of zinc and oxytetracycline in acne vulgaris. Br J Dermatol. 1977 Nov;97(5):561-6.
7. Weimar VM, Puhl SC, Smith WH, ten Broeke JE. Zinc sulfate in acne vulgaris. Arch Dermatol. 1978 Dec;114(12):1776-8.
8. Orris L, Shalita AR, Sibulkin D, London SJ, Gans EH. Oral Zinc Therapy of Acne: Absorption and Clinical Effect. Arch Dermatol. 1978;114(7):1018-1020.
9. Weismann K, Wadskov S, Sondergaard J. Oral zinc sulphate therapy for acne vulgaris. Acta Derm Venereol. 1977;57(4):357-60.
With the popularity of “detox” diets today being what is I’m hoping some people actually want to learn how to increase their body’s natural defenses against toxins using scientifically sound dietary methods, rather than just following one of the many silly “detox juice cleanse” clogging up the internet like a clump of hair stuck in a drain.
With that said let me talk a little about glutathione. Glutathione is a neat little chemical made of 3 amino acids; cysteine, glutamic acid, and glycine. In addition to its role as a strong antioxidant, glutathione plays a very important role in the detoxification process by attaching to various electrophilic toxins, wherein it typically reduces their chemical reactivity and increases their polarity, causing the chemical to be excreted from the body at a greater rate.
The list of toxins to which this process occurs is massive and includes mercury, acrolein, methylglyoxal, and the toxic metabolites of benzo(a)pyrene, 7,12-benzo(a)anthracene, aflatoxin B1, acetominophen, and benzene.
The way glutathione neutralizes these chemicals involves enzymes called Glutathione S-Transferases. These enzymes transfer gluathione onto the dangerous chemicals in question. This review series will look at some dietary factors which support making and using glutathione. It will begin with coffee.
Although coffee is full of hundreds of chemicals, two in particular seem to play the biggest role in coffee’s effect of glutathione. These chemicals are cafestol and kahweol, a pair of lipid soluble diterpenes which are largely removed by paper filters but retained when coffee is made using alternative methods, such as a french press. These chemicals are one of those most heavily studied upregulators of Glutathione S-Transferase and probably explain why french press and italian style coffee increase such enzymes (as well as some other detoxifying enzymes, such as glucoronasyltransferase). In addition, coffee itself seems to increase glutathione itself in various tissues.
These facts may explain why coffee and those two diterpenes, when given to animals, seem to protect against numerous toxins known to be detoxified by glutathione. This may also explain why coffee consumption has been associated with a lower risk of certain cancers, including the liver, one of the primary sites of detoxification.
Although one should be cautious when extrapolating to real life situations, I think their is decent evidence to suggest that coffee, particularly coffee made using a french press or similar devices, has a place in a “detox” diet, should such a thing even be needed in first place (I’ll hold onto my opinions here).
Sreerama L, Hedge MW, Sladek NE. Identification of a class 3 aldehyde dehydrogenase in human saliva and increased levels of this enzyme, glutathione S-transferases, and DT-diaphorase in the saliva of subjects who continually ingest large quantities of coffee or broccoli. Clin Cancer Res. 1995 Oct;1(10):1153-63. PubMed PMID: 9815907.
Esposito F, Morisco F, Verde V, Ritieni A, Alezio A, Caporaso N, Fogliano V. Moderate coffee consumption increases plasma glutathione but not homocysteine in healthy subjects. Aliment Pharmacol Ther. 2003 Feb 15;17(4):595-601. PubMed PMID: 12622769.
Grubben MJ, Van Den Braak CC, Broekhuizen R, De Jong R, Van Rijt L, De Ruijter E, Peters WH, Katan MB, Nagengast FM. The effect of unfiltered coffee on potential biomarkers for colonic cancer risk in healthy volunteers: a randomized trial. Aliment Pharmacol Ther. 2000 Sep;14(9):1181-90. PubMed PMID: 10971235.
Cavin C, Holzhaeuser D, Scharf G, Constable A, Huber WW, Schilter B. Cafestol and kahweol, two coffee specific diterpenes with anticarcinogenic activity. Food Chem Toxicol. 2002 Aug;40(8):1155-63. Review. PubMed PMID: 12067578.
Cavin C, Holzhäuser D, Constable A, Huggett AC, Schilter B. The coffee-specific diterpenes cafestol and kahweol protect against aflatoxin B1-induced genotoxicity through a dual mechanism. Carcinogenesis. 1998 Aug;19(8):1369-75. PubMed PMID: 9744531.
Miller EG, McWhorter K, Rivera-Hidalgo F, Wright JM, Hirsbrunner P, Sunahara GI. Kahweol and cafestol: inhibitors of hamster buccal pouch carcinogenesis. Nutr Cancer. 1991;15(1):41-6. PubMed PMID: 2017397.
THE PROTECTIVE EFFECT OF COFFEE AGAINST PARACETAMOL-INDUCED HEPATIC INJURY IN RATS RENATA VIANA ABREU and TASSO MORAES-SANTOS* Journal of Food Biochemistry Volume 35, Issue 6, pages 1653–1659, December 2011
Gershbein LL. Action of dietary trypsin, pressed coffee oil, silymarin and iron salt on 1,2-dimethylhydrazine tumorigenesis by gavage. Anticancer Res 1994; 14: 1113 6.
Mori H, Kawabata K, Matsunaga K, Ushida J, Fujii K, Hara A, Tanaka T, Murai H. Chemopreventive effects of coffee bean and rice constituents on colorectal carcinogenesis. Biofactors. 2000;12(1-4):101-5. Review.
Johnson, S., Koh, W., Wang, R., Gobindarajan, S., Yu, M., & Yuan, J. (2011). Coffee consumption and reduced risk of hepatocellular carcinoma: findings from the Singapore Chinese Health Study. Cancer Causes & Control, 22(3), 503-10.
Tornai, I. (2010). Role of environmental factors in the etiology of hepatocellular carcinoma. Orv Hetil, 151(28), 1132-6
The following papers include a number of randomized trials in which calcium supplements increased the risk of cardiovascular disease events, including heart attacks:
Bolland MJ, Grey A, Avenell A, Gamble GD, Reid IR. Calcium supplements with or without vitamin D and risk of cardiovascular events: reanalysis of the Women’s Health Initiative limited access dataset and meta-analysis. BMJ. 2011 Apr 19;342:d2040.
Bolland MJ ,Barber PA ,Doughty RN ,Mason B ,Horne A ,Ames R ,et al. Vascular events in healthy older women receiving calcium supplementation: randomised controlled trial. BMJ 2008;336:262
Li S, Na L, Li Y, Gong L, Yuan F, Niu Y, Zhao Y, Sun C. Long-term calcium supplementation may have adverse effects on serum cholesterol and carotid intima-media thickness in postmenopausal women: a double-blind, randomized, placebo-controlled trial. Am J Clin Nutr. 2013 Nov;98(5):1353-9.
Bolland M.J., Avenell A., Baron J.A. et al. Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis. BMJ 2010; 341:c3691.
I’ve posted on this blog about fiber and colon cancer, noting a lack of evidence supporting a protection by fiber on this disease. But what about the effect of fiber on other maladies? What about the condition fiber is supposed to be most effective at treating? Yep, I’m talking about constipation. Here’s a study I came across recently:
Ho KS, Tan CY, Mohd Daud MA, Seow-Choen F. Stopping or reducing dietary fiber intake reduces constipation and its associated symptoms. World J Gastroenterol. 2012 Sep 7;18(33):4593-6.
In this trial, researcher recruited 63 people with constipation. All participants were asked to reduce their fiber intake as low as they could for 6 months. By 6 months 41 subjects were eating almost no fiber, 16 were eating a low fiber diet, and 6 were eating a comparatively high fiber diet. Thus, this was not technically a randomized trial, although the different groups were compared with each other in the style of a controlled trial.
The high fiber group saw no relief of symptoms at all, but they were small in numbers, older, and were clearly poor compliers. Let’s ignore them and look at the low versus almost no fiber groups.
Among those on the low fiber diet, there was a 20 to 30% reduction in the number of people with constipation, anal bleeding, bloating, and abdominal pain. Among the 41 people on the nearly no fiber diets, not a single person had any of these aforementioned symptoms. Everyone who followed this fiber free diet was free from constipation.
This type of study demands further investigation, since it is clearly weak on its own. Still, the results seem incredible. Hopefully future studies will help us determine how legitimate these results are by using a well randomized control group and, ideally, isolating fiber sources (e.g. Soluble and insoluble).