Gaby’s Nutritional Medicine, 2nd Edition, Brims with Clinical Pearls


In today’s era of disposable digital media and ephemeral “alternative facts”, there’s something reassuring about a good old fashioned medical textbook—especially one as thorough and carefully referenced as the new second edition of Dr. Alan Gaby’s landmark work, Nutritional Medicine.

The new edition of this comprehensive compendium first published in 2011, incorporates six additional years of published literature, spanning more than 100 years of nutrition research in total.

Gaby’s experienced eye for the needs of practicing clinicians puts nutrition research into a practical context. Nutritional Medicine highlights evidence backing the use of dietary modifications and nutritional supplements for over 400 different disorders. NutMedTextGaby

Increasingly, patients are seeking nutritional-based therapies to treat their health issues, and the medical community is trying to step up. Gaby believes that’s a very good thing.

At least 30% of all chronic conditions not adequately diagnosed and treated by conventional medicine can be traced to hidden food allergies, Gaby says. He stresses how crucial it is that practitioners not only teach patients how to eat healthfully, but also help them to determine what foods best align with their unique physiology.

When patients make changes appropriate for their particular situations, their healthcare costs frequently drop — and, more significantly, they feel healthier and perform better in life.

No population in history has had as much access to as much medical data as we have today. This leads many patients to believe that they can craft their own self-directed regimens without consulting practitioners. That’s a mixed blessing, for sure.

Self-empowerment and initiative are positive factors for health improvement. But many self-directing patients may be unaware of potentially important drug-nutrient interactions or contraindications related to their medical conditions, Gaby cautions. They also may not always be able to distinguish hype from legitimate science, and they may have difficulty prioritizing which supplements are most likely to help them.

Well-informed holistic practitioners can be invaluable guides in these situations.  With a “careful medical history, a good physical exam, and a working knowledge of the literature,” practitioners can often develop “a safe and effective treatment plan without necessarily ordering a lot of ‘alternative’ lab tests,” says Gaby.

But the key phrase here is “well-informed.”

Gaby’s book represents its author’s lifelong commitment to education. The new and updated edition is an accessible information source for anyone seeking a compilation of clinically relevant nutritional medicine research. The book is available for purchase online at

Here are a few clinical pearls:

Vitamin B3 to Prevent Skin Cancer

A growing body of research indicates that oral supplementation with niacinamide (vitamin B3) may prevent the development of skin cancer.

A common health condition, non-melanoma skin cancer (NMSC) — including basal cell and squamous cell carcinoma — often develops from precancerous actinic keratoses. Ultraviolet (UV) irradiation-induced immunosuppression is thought to play a role in this transformation. Immunosuppression can occur with UV doses well below the sunburn threshold, and may not be effectively prevented by sunscreen.

In two studies, healthy volunteers who received a single topical application of 5% niacinamide lotion1 or an oral vitamin B3 supplement (500 mg once or 3 times per day for 7 days)2 demonstrated significantly decreased degrees of UV induced immunosuppression. Niacinamide also enhanced the repair of UV-induced DNA damage in both human keratinocytes — the predominant cell type in the epidermis — and melanocytes in vitro3, 4, suggesting another mechanism by which this vitamin might help to prevent skin cancer.

Additionally, results from a double-blind trial showed that topical application of 1% niacinamide gel twice a day appeared to accelerate the resolution of actinic keratoses in elderly patients.5 In other double-blind studies of patients with actinic keratoses, with or without a history of NMSC, oral administration of niacinamide (500-1,000 mg per day) decreased the number of actinic keratoses and reduced the number of new skin cancers.

Healthy individuals (aged 48-90 years) with sun-damaged skin and at least 4 actinic keratoses were randomly assigned to receive, in double-blind fashion, oral niacinamide or placebo for 4 months. In trial 1, 18 patients received 500 mg of niacinamide twice a day and 17 received placebo. In trial 2, 21 patients received 500 mg of niacinamide once daily and 20 received placebo. The patients were encouraged to use sunscreen. After 4 months, compared with placebo, niacinamide reduced the number of actinic keratosis by 35% (p < 0.001) in trial 1 and by 29% (p = 0.005) in trial 2. In the combined trials, 11 placebo-treated patients developed 20 new skin cancers (12 basal cell carcinoma [BCC] and 8 squamous cell carcinoma [SCC]), and 2 niacinamide-treated patients developed 4 skin cancers (2 BCC and 2 SCC). The proportion of patients who developed at least 1 new skin cancer was 86% lower (p < 0.02), and the total number of new skin cancers was 76% lower (p = 0.01) with niacinamide than with placebo.6

In another study, 386 individuals (mean age, 66 years) with at least 2 NMSCs in the previous five years (mean, 8; range, 2-61) and a mean of 47 actinic keratoses at baseline (range, 0-214), were randomly assigned to receive, in double-blind fashion, 500 mg of niacinamide twice a day or placebo for 12 months. At 12 months, the mean number of new NMSCs (basal cell and squamous cell carcinomas) was significantly lower by 23% in the niacinamide group than in the placebo group (1.8 vs. 2.4; p = 0.02). The number of prevalent actinic keratoses was 11% lower in the niacinamide group than in the placebo group at 3 months (p = 0.01), 14% lower at 6 months (p < 0.001), 20% lower at 9 months (p < 0.001), and 13% lower at 12 months (p = 0.001). During the 6 months after treatment was discontinued, the mean number of new NMSCs was 0.8 in each group, indicating that the benefits of niacinamide did not persist after the treatment was discontinued. No significant side effects occurred.7

In a final study, 24 patients with actinic keratoses who had undergone kidney transplant were randomly assigned to receive niacinamide (250 mg 3 times per day) or placebo. After 6 months, 88% of the patients receiving niacinamide had partial regression of some or all actinic keratoses, and in 44% of the patients some of the areas showed complete regression. No improvement was seen in the placebo group.8

Long-term prophylaxis with oral niacinamide — and possibly with topical niacinamide as well — seems worthwhile for patients with actinic keratoses or a history of non-melanoma skin cancer.

  1. Damian DL, Patterson CRS, Stapelberg M, et al. UV radiation-induced immunosuppression is greater in men and prevented by topical nicotinamide. J Invest Dermatol 2008;128:447-454.
  2. Yiasemides E, Sivapirabu G, Halliday GM, et al. Oral nicotinamide protects against ultraviolet radiation-induced immunosuppression in humans. Carcinogenesis 2009;30:101-105.
  3. Surjana D, Halliday GM, Damian DL. Nicotinamide enhances repair of ultraviolet radiation-induced DNA damage in human keratinocytes and ex vivo skin. Carcinogenesis 2013;34:1144-1149.
  4. Thompson BC, Surjana D, Halliday GM, Damian DL. Nicotinamide enhances repair of ultraviolet radiation-induced DNA damage in primary melanocytes. Exp Dermatol 2014;23:509-511.
  5. Moloney F, Vestergaard M, Radojkovic B, Damian D. Randomized, double-blinded, placebo controlled study to assess the effect of topical 1% nicotinamide on actinic keratoses. Br J Dermatol 2010;162:1138-1139.
  6. Surjana D, Halliday GM, Martin AJ, et al. Oral nicotinamide reduces actinic keratoses in phase II double-blinded randomized controlled trials. J Invest Dermatol 2012;132:1497-1500.
  7. Chen AC, Martin AJ, Choy B, et al. A phase 3 randomized trial of nicotinamide for skin-cancer chemoprevention. N Engl J Med 2015;373:1618-1626.
  8. Drago F, Ciccarese G, Parodi A. Nicotinamide for skin-cancer chemoprevention. N Engl J Med 2016;374:789-790.

N-Acetylcysteine Improves Success Rate of Helicobacter pylori Treatment

In the past few decades, it has become apparent that recurrences of peptic ulcers can be prevented by eradicating Helicobacter pylori. Treatment with a combination of antibiotics, acid blockers (proton pump inhibitors) and sometimes bismuth is often effective — but in a substantial minority of patients the infection persists despite treatment. New research has shown that supplementation with N-acetylcysteine prior to attempted eradication therapy substantially increases the success rate.

H. pylori produces a protective biofilm. Biofilms are thought to promote antibiotic resistance by several different mechanisms, one of which is to block the penetration of antibiotics. N-Acetylcysteine (NAC) has been found to prevent biofilm formation in vitro and to promote the degradation of existing biofilm.1 In clinical trials, supplementation with NAC markedly increased the success rate of conventional eradication therapy, both in patients undergoing their first course of treatment and in those who had previously had multiple unsuccessful attempts.

Forty patients who had had at least 4 unsuccessful attempts to eradicate H. pylori were randomly assigned to receive NAC (600 mg once a day) or no NAC (controls) for 1 week, followed by a culture-guided eradication regimen that included 2 antibiotics and a proton pump inhibitor. The eradication rate was significantly higher in the NAC group than in the control group (65% vs. 20%; p < 0.01). Biofilm disappeared in all patients in whom eradication was successful, but persisted in patients in whom eradication failed.2

In another study, 70 patients with H. pylori infection were randomly assigned to receive 500 mg of clarithromycin and 30 mg of lansoprazole, each twice a day, with or without 10 ml (400 mg) of NAC liquid 3 times per day for 10 days. Eradication of H. pylori was assessed 1 month after the completion of treatment via rapid urease test on gastric biopsy samples. The eradication rate was significantly higher in the NAC group than in the control group (50% vs. 23%; p = 0.034).3

 Adjunctive treatment with NAC should be considered for all patients undergoing H. pylori eradication therapy.

  1. Dinicola S, De Grazia S, Carlomagno G, Pintucci JP. N-acetylcysteine as powerful molecule to destroy bacterial biofilms. A systematic review. Eur Rev Med Pharmacol Sci 2014;18:2942-2948.
  2. Cammarota G, Branca G, Ardito F, et al. Biofilm demolition and antibiotic treatment to eradicate resistant Helicobacter pylori: a clinical trial. Clin Gastroenterol Hepatol 2010;8:817-820.e3.
  3. Gurbuz AK, Ozel AM, Ozturk R, et al. Effect of N-acetyl cysteine on Helicobacter pylori. South Med J 2005;98:1095-1097.

CoQ10 Reduces Mortality Rate in CHF Patients

Coenzyme Q10 (CoQ10) substantially reduces the mortality rate in patients with congestive heart failure. CoQ10 as a treatment for heart failure is not new, but the research to date has been conflicting, and most of the studies did not investigate mortality. The most recent study–published in 2014– study was well designed and was one of the largest studies of CoQ10 for heart failure.

A cohort of 420 patients (mean age, 62 years) with chronic heart failure (88% in New York Heart Association [NYHA] class III) were randomly assigned to receive, in double-blind fashion, 100 mg of CoQ10 3 times per day or placebo, in addition to standard therapy, for 2 years. The proportion of patients who reached the composite endpoint of hospitalization due to worsening heart failure, cardiovascular death, or urgent heart transplantation and mechanical support was significantly lower by 43% in the CoQ10 group than in the placebo group (14.9% vs. 26.1%; p = 0.003). Cardiovascular mortality (9% vs. 16%; p = 0.026), all-cause mortality (10% vs. 18%; p < 0.02), and incidence of hospitalization for heart failure (8% vs. 14%; p = 0.033) were significantly lower in the CoQ10 group than in the placebo group. The proportion of patients who showed an improvement in NYHA class after 2 years was significantly greater in the CoQ10 group than in the placebo group (58% vs. 45%; p < 0.03).1

  1. Mortensen SA, Rosenfeldt F, Kumar A, et al. The effect of coenzyme Q10 on morbidity and mortality in chronic heart failure. Results from Q-SYMBIO: a randomized double-blind trial. JACC Heart Fail 2014;2:641-649.

High-Dose Vitamin D Inappropriate in Many Cases

It is common practice among many holistic practitioners to measure vitamin D levels (25-hydroxyvitamin D) in the blood and to recommend relatively large doses of vitamin D in order to bring the blood level to a purported “optimal” range. While on face value this seems reasonable,  high-dose vitamin D may be inappropriate in many cases.

Advocates of high-dose vitamin D point out that RDA levels of vitamin D often fail to achieve vitamin D “sufficiency” (defined as a serum 25[OH]D level ≥ 30 ng/ml). They also argue that supplementing to achieve an optimal serum 25(OH)D level can produce a wide range of health benefits. Furthermore, they claim that up to 10,000 IU per day of vitamin D is generally safe for long-term use, and that even higher doses are safe as long as the serum 25(OH)D level is not too high. Their definition of “excessive” ranges from 80-150 ng/ml.

Based on the literature, however, the clinical value and cost-effectiveness of 25(OH)D testing is questionable. In the absence of severe vitamin D deficiency or toxicity, serum 25(OH)D appears to be an unreliable indicator of actual vitamin D status. The evidence supporting the idea of increasing 25(OH)D beyond the reference range of 10-15 ng/ml is weak. Further, raising the bottom limit of the “normal” range to 30 ng/ml–as many laboratories have done–may substantially overestimate the prevalence of vitamin D deficiency. The appropriate 25(OH)D reference range may be different for different racial/ethnic groups.

High-dose vitamin D supplementation may, in some instances, cause more harm than good. Formation of kidney stones is one potential side effect of vitamin D overconsumption. Long-term safety of supplementation at doses greater than 2,000 IU per day has not been established.

“There are many examples in nutritional medicine where more is better,” Gaby says. “But the available evidence suggests that that may often not be the case with respect to vitamin D.” For most patients who might benefit from increased vitamin D intake, he recommends supplementing with 800-1,200 IU per day, without measuring 25(OH)D levels.

The second edition of Gaby’s Nutritional Medicine textbook is available for purchase online at


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