20 July 2014 HIGH CARBS OR LOW CARBS? THE BIG FAT SURPRISE – which is best for weight loss? a collaborative literature metanalysis study July 2014 by Naude ea the universities of Stellenbosch, Cape Town and Liverpool (UK) claimed to compare the effects of low CHO and isoenergetic balanced weight loss diets in overweight and obese adults, stratified by outcomes at 3-6 months and 1-2 years. Of nineteen trials (n = 3209), 3 had adequate allocation concealment. In non-diabetic participants, analysis showed little or no difference in mean weight loss in the two groups at 3-6 months (MD 0.74 kg) or for blood pressure, LDL, HDL and total cholesterol, triglycerides and fasting blood glucose. In diabetic participants, findings showed a similar pattern. CONCLUSIONS: Trials show weight loss in the short-term irrespective of whether the diet is low CHO or balanced. There is probably little or no difference in weight loss and changes in cardiovascular risk factors up to two years of follow-up when overweight and obese adults, with or without type 2 diabetes, are randomised to low CHO diets and isoenergetic balanced weight loss diets.
‘But Noakes points out, Low-fat, high-carb, high-sugar diet a likely cause of obesity/diabetes “I refer to the report in the Cape Times of July 10, “Noakes’s popular low-carb diet is not healthier, better for weight loss – study “. Since the authors of that study (Naude ea) do not understand either what constitutes a low-carbohydrate diet or the unique biological effects of such diets, they were predisposed to produce a biased report that comes to exactly the wrong conclusion.
‘First, the conclusion of their study was predictable since the authors chose to review only studies in which subjects ate the same number of calories on both diets. It is not clear how the authors conceived that diets that provided exactly the same number of calories would produce different outcomes. Indeed, a core teaching of these nutritional scientists is that the degree of weight loss is determined by the reduction in calorie consumption. Thus the authors knew the outcome of their study even before they undertook it. This is not good science.
‘Second, the studies included in their meta-analysis are not of the low-carbohydrate diet described by either Dr Robert Atkins or ourselves in Real Meal Revolution. Dr Atkins realised in the 1970s that the majority of overweight/obese persons can only reduce their weights successfully, and keep that weight off in the long term, if they eat less than 60g carbohydrate/day for the rest of their lives. Higher intakes are increasingly less effective. In Real Meal Revolution we stress that those with insulin resistance/ type 2 diabetes need to keep their carbohydrate intakes even lower, ideally to about 25g/day. The “low-carbohydrate ” diets included in the meta-analysis provided a minimum of 200g carbohydrate/day (or 4-8 times higher than the carbohydrate content that is known to be effective). As a result this is a meta-analysis of studies providing a high, not a low-carbohydrate load for those with obesity/insulin resistance/type 2 diabetes.
‘Third, the extent of weight loss in the studies included in he meta-analysis is small, the greatest values being about 10kg. For most people with significant weight problems, such small weight losses are probably relatively meaningless and should be classified a diet failure, not a success. But freeliving persons who follow individually prescribed carbohydrate diets providing about 25g carbohydrate/day report quite remarkable degrees of weight loss, not infrequently up to 40-80kg, usually achieved effortlessly if the low-carbohydrate rules are followed.
‘Fourth, the unique biological effects of the properly-defined low-carbohydrate is that (i) It reduces hunger, allowing subjects to eat fewer calories without experiencing continual hunger. The point, as stressed by Dr Atkins, is that the low-carbohydrate diet is a low-calorie, no-hunger diet. (ii) The diet lowers blood insulin concentrations. In those with obesity/insulin resistance/metabolic syndrome, it is continually elevated blood insulin concentrations that cause ill-health (as clearly established by the work of Dr Gerald Reaven of Stanford University over the past 50 years).
‘The authors found that health benefits were no different on either diet. A number of properly designed, peer-reviewed meta-analyses of the real low-carbohydrate diets show that weight loss and health benefits are superior compared with higher-carbohydrate diets. Unfortunately, the authors appear to be ignorant of those studies since neither they nor your reporter refers to them. This implies the presence of bias, questioning the true intent of the report.
‘The report also includes the statement of the Heart Foundation of South Africa (HFSA) to the effect that a diet high in saturated fat causes heart disease. Unfortunately, the HFSA spokesperson appears unaware of Nina Teicholz’s recentbook, The Big Fat Surprise: Why Butter, Meat, Cheese Belong in Healthy Diet, and the June 23 Time Magazine Ending the War on Fat, which show that this dogma is false and is not based on any credible science. It is time the HFSA updated its understanding of what actually causes heart disease. They might also want to consider whether their promotion of their unproven low-fat, high-carbohydrate, high sugar diet for the past 37 years is the most likely direct cause of the obesity/diabetes epidemic that has since engulfed South Africans.
‘Indeed on a practical side, I wonder if the authors have ever considered studying the dietary intakes of the obese diabetic patients they treat at Tygerberg and Groote Schuur hospitals. Do patients with these diseases eat either high- or low-carbohydrate diets? Why is is that these twin diseases, which are crippling the health services of the Western Cape, began to increase exponentially only after the 1977 Dietary Guidelines that institutionalised the low-fat, high-carbohydrate diets? Surely these are the critical questions that should really be exercising the minds of the Western Cape’s nutritional scientists? The best conclusion that can be drawn from this study is that diets providing more than 10 percent of daily calories in the form of carbohydrate are equally ineffective in producing meaningful degrees of weight loss in those with obesity/insulin resistance/type 2 diabetes.”
15 June 2014 DIET RISKS FOR BREAST CANCER, INFECTION & ALL ELSE: Sugar? Fats? Vitamins?
VITAMIN INTAKE, INFECTION, BREAST CANCER:
IT IS COMMON CAUSE THAT ONE DOESNT, CANNOT PREVENT OR TREAT INFECTION BY POOR NUTRITION OR LOWDOSE ANTI- MICROBIALS- such policy is futile if not dangerous for breeding resistance as well as disease extension. The studies below confirm the obvious, (as Klenner, Pauling, Cameron ea showed the past 50 years with highdose vit C injection), that vitamin D3 orally also works as a multiantimicrobial agent if given as early as possible in safe very high dose and bloodlevel eg 600 000iu monthly (in the first month, – in Salhuddin’s Pakistan PTB patients (presumably also Sunni muslim) initially mean wt 45kg, thats vit D3 ~440iu/kg/d) for two doses ie a mean of 300iu/kg/day over 90days; not the current preventative recommendation of 80iu/kg /day to a safe blood level of around 50-60ng/ml. As Holick has said, with adequate water intake even 50 000iu vit D3 a day ie 1.5million iu/month for months causes no toxicity. Given the 40% mortality rate in the frail Saudi MERS patients, and in acute severe influenza and other serious viral infections, it can be expected that such highdose immediate vitamin D3 therapy orally with eg 600 000iu, combined with highdose vitamin C, zinc and some multivite, (never mind appropriate antibiotics in acute bacterial infection) will similarly virtually eliminate mortality.
But no KSA Govt website mentions this- except the Saudi Gazette a year ago which strongly urged vitamin D supplement in the KSA as even daily sun exposure does not bring most Saudi women above the vitamin D deficiency threshold. It says Since Muslim women can only reveal the hands and face, they may need to be out in the sun for longer than 30 minutes. But the review conspicuously fails to mention that in public outdoors in KSA, women must have even the head and face covered. It also propagates surprising dangerous nonsense that “severe deficiency needs monthly vitamin D injection – “Mom, have you taken your vitamin D injection this month?, when all it requires is an oral daily, weekly or fortnightly dose vitamin D3 at trivial cost.” It does stress “One of the main reasons why vitamin D deficiency is so common in the Kingdom is because there are very few food sources of vitamin D. Foods which have fairly good amounts of vitamin D are fish liver oil, sweet potatoes, egg yolks, vegetable oils, butter, and fatty fish such as salmon, sardines, and tuna,” said Dr. Rasha Jameel, a consultant in family medicine at a local hospital. In the United States, all milk and dairy products are fortified with vitamins A and D, but no such measures are in place in the Kingdom“.
This correlates with a new metaanalysis (in the BMJ this month) of observational studies from Europe and USA, that all-mortality hazard ratio over a mean of 10 years increases by 57% as vit D level falls from the highest to the lowest level. The KSA apparently chooses to ignore that, as this column reported recently from WHO data, despite apparently being the wealthiest country per capita of bigger populations in the world, KSA’s population life expectation is about 5 years lower than eg far less sunny Britain’s; ie KSA all-cause mortality rate is avoidably materially higher. Despite KSA medical professors having reported in studies that most of the KSA population is deficient in vits D and C, the KSA Govt website chooses to ignore this on official websites; unlike other even Middle-Eastern governments promoting vit D fortification or meaningful safe supplements costing trivial amounts.
Even a new study last year from KSA universities confirmed that ” Most commonly consumed food products by Saudi population which are supposed to be fortified by vitamin D are either not fortified or contain an amount less than (apparently from their table 2 ~ half of) recommended by guidelines set for US marketplace”. Even a UAE authority recently stressed “Can fortified milk fight Vitamin D deficiency? Shockingly low levels of D3 among UAE population cannot be rectified by milk alone.” As Holick ea, including a Turkish University 2010 trial report, oral vitamin D3 is far more effective , and safer than, either vitamin D2, or vitamin D injection -never mind much cheaper. This current ostrich-head-in-the-sand denialism by the KSA government is like that of the RSA govt under Presidents Mbeki and Zuma 10-15 years ago about preventing and treating HIV-AIDS – considering that the safe and beneficial daily intake of vitamin D3 is now universally recognized as 4000 if not 10 000iu/day (ie about 80iu/kg/day or pro rata up to perhaps fortnightly) , to a mean blood vit D level of about 60 to 80ng/ml. .
As Prof Mike Holick pointed out a few years ago, “Even in Saudi Arabia, Qatar and South Africa, more than 50% of the population is deficient in vitamin D, all because of their avoidance of sun. Based on some of the literature, it seems that we could probably decrease health care costs across the board by 25% if everybody had optimal vitamin D status.” As Al Faraj ea reported in Riyadh in 2003, Prof Zahid Naeem from a KSA university wrote in 2010, “Vitamin D deficiency is an ignored epidemic in KSA and globally“; confirmed by a KSA study by Ali ea in 2012: “Even in a sunny country like Saudi Arabia the prevalence of vitamin D deficiency in young female is high“.. One does not need to speculate why the KSA and all governments globally choose to ignore this inconvenient truth, downplay effective vigorous vitamin C and D3 (sunshine) supplements- such widespread vitamin D and C deficiencies, like cigarette smoking and alcohol abuse, suit governments and Big Pharma- the Disease Industry- in reducing populations growths and creating jobs for the highly profitable Disease Industry and it’s shareholders- for whom Only Disease Pays. Cheap safe natural Prevention Does not Pay since it at least halves sickness never mind disease industry jobs, taxes and profiteering in the global $multitrillion Disease and Diet and Vaccine and Invasive Screening Industry scams.
And Karen Hansen ea at Univ Wisconsin 2014 have just shown that giving vitamin D2 (not D3) 50 000iu fortnightly for a year is actually adverse – as Holick and others have show – IT DEPRESSES – perhaps halves – THE BIOLOGICALLY ACTIVE blood 25OHVIT D3 while boosting perhaps 5 fold the far less active blood 25OHvit D2 levels , and actually worsens rheumatoid arthritis clinically and serologically . One can speculate whether vit D2 actually blocks optimal function of VDRs vitamin D receptors. Trials published 2012 from Japan and Netherlands showed that vitamin D3 – blood 1,25(OH)2D3 (but not TNFalpha blockers) blocked inflammation (ie TNF tumour necrosis factor alpha activation of vascular calcification).
Salahudfin ea’s new randomized controlled trial from Pakistan Vitamin D3 injection accelerates clinical recovery from tuberculosis shows “impressive clinical (weight gain, chest xray and sputum clearing) improvement over 3 months on outpatient TB therapy (Directly Observed Therapy (DOTS) with 2months of 4 antituberculous drugs [Isoniazid, Rifampicin, Ethambutol and Pyrazinamide] followed by 6months Isoniazid and Ethambutol) with two doses 600 000iu vit D3 imi (vs placebo inj) a month apart- ie equivalent to about 7 000iu/day over the 3 months treatment period . This dose of vitamin D is as recommended for vitamin D supplement by the Pakistan Endocrine Society. Trough 25OH vit D levels increased from about 20 to 90ng/ml. After 12weeks, the vitamin D supplemented pts (mean 28 yrs, BMI 17.2kg, 85% moderate to far advanced lung disease) had significantly greater mean weight gain (kg)+3.75, (3.16 – 4.34) versus+2.61, p 0.009; lesser residual disease by chest xxray- 30% fewer zones involved 1.35 v/s 1.82 p 0.004, and 50% or greater reduction in cavity size 106 (89.8%) v/s 111 (94.8%), p 0.035. Vitamin D supplementation led to significant increase in MTBs-induced IFN-g secretion in patients with baseline ‘Deficient’ vitamin D serum levels (p 0.021). Patients in the vitamin D arm and serum < 30 ng/mL (‘Insufficient’ and ‘Deficient’ groups) at enrollment had significantly greater improvements in TB severity scores compared to patients with normal baseline vitamin D levels; p 0.014. This corresponds with the earliest reports of the benefits of vitamin D in TB patients published in 1848  that describes disease arrest, weight gain and reduction in mortality in patients with TB treated with cod liver oil compared to standard therapy alone. More recently, Martineau et al  demonstrated that a single oral dose of 2.5mg (100,000IU) of vit D2 significantly reduced growth of mycobacteria . A randomized, placebo controlled study on 67 Indonesian patients, by Nursyam et al , Jakarta  reported that pulmonary TB patients given 420,000IU of vitamin D over 6weeks ie 10 000iu/day had significantly higher sputum conversion rates as compared to placebo (p 0.002). Martineau et al.  showed that 100,000 IUs of 25-hydroxyvitamin D3 supplementation significantly improved sputum conversion rates in patients with the Taq1 25-hydroxyvitamin D receptor polymorphism of the tt genotype. .
As Salahuddin ea note, the good results in Pakistan in only 3 months with vigorous INITIAL dose vit D3 contrasts with Two recently published large randomised, controlled trials of conservative vitamin D3 over months that achieved far lower blood vitamin D levels found no difference in clinical outcomes or mortality after 400,000IU of 25-hydroxyvitamin D3 or placebo were given by Martineau ea in London, UK to 146 pulmonary TB patients – where mean (trough or midpoint) vit D level (after 100 000iu vitamin D(3) or placebo at baseline and 14, 28, and 42 days after starting standard tuberculosis treatment) – was surprisingly only 40ng/ml at 56days – ie after a mean of 7000iu/d by 56 days, vs 10ng/ml on placebo)- less than half of the bloodlevel achieved on vit D3 in the Pakistan trial ;
and by Wejse et al 2009 in Guinea-Bissau to 365TB patients – who received 300,000 IUs of vit D3 ie only 100,000 IU or placebo at inclusion and again 5 and 8 months after the start of treatment, ie below 1000iu vit D3 per day over the 12 month trial period “. The Guinea-Bisseau pts thus might have achieved a mean blood vit D level boost of only 10ng/ml.. and now Havers ea (Baltimore) show Low 25(OH)D is common in diverse HIV-infected populations and is an independent risk factor for clinical and virologic failure; Low 25(OH)D was associated with high body mass index (BMI), winter/spring season, country-race group, and lower viral load. Baseline low 25(OH)D was associated with increased risk of human immunodeficiency virus (HIV) progression and death (adjusted hazard ratio (aHR) 2.13; 95% confidence interval [CI], 1.09–4.18) and virologic failure (aHR 2.42; 95% CI, 1.33–4.41). and Shepherd ea (Eurocoord) Low Vitamin D predicts short term mortality in HIV-positive persons Odds of death decreased by 46.0%( P = .04) for a 2-fold increase in latest 25(OH)D level.. In patients with current 25(OH)D <10 ng/mL, hsIL-6 concentration increased by 4.7%(95% CI, .2,9.4, P = .04) annually after adjustment for immunological/inflammatory markers, and no change in hsCRP rate was observed (P = .76)