PUFA Increases Postprandial Thermogenesis in Healthy Premenopausal Women & Beyond – 14% Increase Over MUFA & SFA Sounds Huge, But Does it Matter?

Is there something to the good vs. bad fat shenanigan, after all?

Only recently scientists from the Texas Tech University report that a PUFA-rich high-fat meal led to a greater diet-induced thermogenesis in normal-weight premenopausal women compared with SFA- or MUFA-rich high-fat meals.

Reason enough to take a closer look at this and previous studies investigating the diet-induced thermogenic effects of PUFA-, MUFA- and SFA-rich meals and to conduct a reality check wrt to the question whether these differences actually matter – I mean, will you get and stay lean by upping your PUFA intake? Let’s take a look!

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In the initially mentioned study, Hui C. Clevenger, Amanda L. Kozimor, Chad M. Paton and Jamie A. Cooper explored the effect of three HF meals enriched with different fatty acids (MUFAs, PUFAs or SFAs) on metabolism in premenopausal women of normal weight. In that, the metabolic parameters of interest included postprandial energy expenditure (EE), which is then used to calculate DIT, and substrate oxidation, which included respiratory exchange ratio (RER), fat oxidation and carbohydrate (CHO) oxidation.

Based on previous research in men of normal weight, the Texas Tech researchers hypothesized that the diet induced thermogenesis (DIT) and fat oxidation would be the highest after the PUFA- and MUFA-rich meals and lowest after the SFA-rich meal in premenopausal women – a result of which you already know that it was only partly confirmed.

Figure 1: Diet-induced thermogenesis and respiratory exchange rate (higher RER = lower fatty acid oxidation vs. higher CHO oxidation) in the 5h after the test meal (Clevenger. 2014)

The data in Figure 1 does after all tell you that the expected MUFA-induced increase in diet-induced thermogenesis did not occur. PUFAs, on the other hand did the job, Clevenger et al. expected them to do. They increased the DIT by an ostensibly whopping 14% over the DIT the scientists observed in response to the ingestion of the high MUFA and SFA liquid meals that had been prepared with the same base of 8 fl oz (237 ml) of chocolate Ensure(R) with soy lecithin and Nesquik (R, but contained different additional dietary fatty acids added depending on the treatment condition:

  • Table 1: Liquid meal nutrient composition
    breakdown (Clevenger. 2014).

    The PUFA-rich meal was ‘base’ plus sunflower oil and flaxseed oil, with 42% of total energy coming from PUFA.
     

  • The MUFA-rich meal was ‘base’ plus canola oil and extra virgin olive oil, with 42% of total energy coming from MUFA.
  • Finally, the SFA-rich meal was ‘base’ plus butter, coconut oil and palm oil, with 40% of total energy coming from SFA. 

As the data in Table 1 indicates, the nutrient profiles didn’t differ much. The fatty acid composition, on the other hand did, with the SFA meal being the only one with measurable amounts of Butyric, Caprioc, Caprylic, Capric, Lauric, Myristic and Hepatedic acid. Fatty acids of which previous research indicate that they induces an obesity-linked proinflammatory gene expression profile in adipose tissue of subjects at risk of metabolic syndrome (van Dijk. 2009).

High MUFA diets, on the other hand, have been shown to potentiate the effects of weight loss in obese NIDDM patients (Low. 1996). They are the major group of fatty acids in the one oil, everyone appears to agree that it’s health (Olive oil). And last but not least, even the allegedly unhealthy omega-6s have been shown in randomized controlled to reduce liver fat and modestly improve metabolic status, without weight loss, when compared to high saturated fat diets (Bjermo. 2012).

All of these effects / this evidence could potentially be more important than the increase postprandial thermogenesis in the study at hand – so the ultimate question is: Does DIT even matter?

Now, does this increase in DIT matter? Westerterpet et al. who found a negative correlation between body fat levels and the diet induced thermogenesis in their 2008 study (Westerterpet al. 2008), certainly believe it matters. If we look at the total extra diet-induced energy expenditure in 5h after the test-meal in the study at hand, on the other hand, I cannot but ask myself, whether those 1.4kcal can actually make a difference.

I am not sure what you think, but considering the fact that you can burn those 1.4 extra calories in less than one minute in the gym, it’s hard to believe that the increased thermogenesis alone warrants the layman’s conclusion that the study at hand would provide evidence for the superiority ot PUFAs over MUFAs and saturated fats … what do you think?

References:

  • Bjermo, Helena, et al. “Effects of n− 6 PUFAs compared with SFAs on liver fat, lipoproteins, and inflammation in abdominal obesity: a randomized controlled trial.” The American journal of clinical nutrition 95.5 (2012): 1003-1012.
  • Clevenger, Hui C., et al. “Acute effect of dietary fatty acid composition on postprandial metabolism in women.” Experimental physiology (2014): expphysiol-2013.
  • Westerterp, Klaas R., et al. “Dietary fat oxidation as a function of body fat.” The American journal of clinical nutrition 87.1 (2008): 132-135.

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ARNOLD’S BLUEPRINT FOR MAMMOTH SHOULDERS AND ARMS

No bodybuilder was as renowned as Arnold for his huge arms and massive delts. And no bodybuilder trained as hard. Here's a peek at how Arnold's high-volume, high-frequency approach made him the world's greatest bodybuilder. Part 4 of a 4-part series.

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“Honey, I Shrunk The Kardashians!”

What's wrong with Kim Kardashian's latest gizmo? It's a cinch to explain.

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Curcumin, Genistein, Pomegrenate & Co. – A Dirty Dozen of Supplements & Foods to Keep Your Prostate Cancer Free

Which of the dirty dozen of supplements and foodstuffs in today’s SuppVersity review can really help you to make sure, you’re not the one out of those nine men who develops prostate cancer?

Supplements that are supposed to protect you from developing prostate cancer and/or agents that may help patients with existing prostate issues are – obviously – in high demand. And as W. Merkle points out in a recent article in the German science journal Urologe using them – even if they may not be as effective as some patients may believe – makes sense: from a psychological perspective, alone (Merkle. 2014).

Taking a pill with selenium, for example, has been shown to alleviate some of the side effects of chemotherapy. General protective effects against prostate cancer, on the other hand, have not been established. In fact, the most recent studies rather suggest that “supplementation did not benefit men with low selenium status but increased the risk of high-grade PCa among men with high selenium status” (Kristal. 2014).

Supplements are nice, but without exercise you are missing 50% of the anti-cancer equation!

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Luckily, there are other supplements with more promising data. Supplements that will actually complement, a healthy diet and active lifestyle, the two pillars of all (not just prostate) cancer protection. Supplements like…

  • Curcumin – As a SuppVersity reader you’ve probably already expected to see the curcumin on the list. Its potent anti-inflammatory effects and more specifically its ability to target multiple inflammatory pathways, which include NF-KappaB, COX2, STAT3 and high levels of CRP, Prostaglandins and TNF-alpha make it a particularly valuable anti-tumor agent of which Guo et al. observed in a recent study that it will induce cell cycle arrest and apoptosis of prostate cancer cells by regulation the expression of IkappaBalpha, c-Jun and androgen receptor (Guo. 2013)
  • Genistein – Just like curcumin, genistein acts on NF-KappaB (Adjakly. 2013). In addition it will upregulate a protein called miR-574- 3p that will have cancer cells “kill themselves” (go into apopotosis; Chiyomaru. 2013). In addition scientists have found genistein to support the efficiacy of Cabazitaxel which is used for the treatment of hormone-refractory prostate cancer.
  • Pomegranate - Pomegranate extracts or rather its ingredients, i.e. ellagic acid, caffeic acid, luteolin and punicic acic, have been shown to inhibit the proliferation and induce apoptosis in prostate cancer cells (NCI. 2013).
    Figure 1: If you look at the actual increase in apoptotic cancer cells in response to the pomegranate treatment, it is obvious that some patients (e.g. #53) benefited more than others (Pantuck et al. 2006)

    A clinical trial by Pantuck et al. (2006) was also able to show that the time it takes for the PSA levels, an albeit debatable marker of prostate cancer risk, to double decreased significantly, when the subjects, men with rising PSA after surgery or radiotherapy, were treated with 8 ounces of pomegranate juice daily (Wonderful variety, 570 mg total polyphenol gallic acid equivalents) until disease progression. Unfortunately, a more recent study by Stenner-Liewen et al. (2013) could not confirm these effects. 

  • Brassica vegetables (cruciferous vegetables) – While general vegetable intake is already associated with a -39% reduced risk of developing extraprostatic prostate cancer (cancer, eating tons of cruciferous vegetable, it was the intake of broccoli and cauliflower that made the biggest impact in a 2007 study by Kirsh et al.
    Even if they don’t protect you from prostate cancer broccoli & co will inhibit myostatin and could help you to grow more muscle… well, at least theoretically, you know about the difference between the petri dish and the real world, so don’t expect monster gains | more.

    As it is usually the case the evidence is yet ambiguous. In a 2002 review of the evidence, Kristal, et al. found that of the six studies they could clearly interpret, only three reported statistically significant reduced risks (P < 0.05), while one reported a borderline significant reduced risk (P = 0.06). Against that background Verhoeven et al. are right, when they say: ” Further epidemiological research should separate the anticarcinogenic effect of brassica vegetables from the effect of vegetables in general” (Verhoeven. 1996).

    More recently, Joseph et al. found that the existing differences in the epidemiological data may be due to genetic polymorphisms due to which only men with a certain genetic polymorphisms in glutathione S-transferases M1 and T1 will benefit from eating tons of cruciferous veggies (Joseph. 2004).

  • Green tea – Green tea is good for everything, right? Well unless it’s not loaded with toxic molecules (see previous SuppVersity article) this may in fact be right. Convincing evidence from human trials is albeit scarce. What we do have are rodent studies like the ones that were conducted with TRAMP mice, which model closely mirrors the pathogenesis of human prostate cancer.

    In these mice EGCG, one of the main catechins in green tea, decreased the proliferation of prostate cancer cells and reduced the PSA levels. Scientists believe that these effects are mainly mediated by the effects EGCG has on the growth promoting proteins ERK1/2. Unfortunately, the same rodent studies also suggest that it is probably too late for many of you to start drinking green tea, now, because said beneficial effects are only observed in young, not in old TRAMP mice (Donald. 2012).


  • Coffee is for the ladies, too! Studies show significantly reduced risks of breast cancer with 5+ cups of coffee. Tee and cacao help, as well | more

    Coffee - Obviously I am biased, when it comes to coffee. I still hope you believe me when I say that drinking 5+ cups of coffee per day has been associated with significantly reduced risk of prostate cancer in what is probably the most large-scale meta-analysis of the topic today.

    In their meta-analsis of 12 peer-reviewed case-control studies, Lu et al. calculated a 4% risk reduction for Europeans who consumed five or more cups of coffee and Americans who consumed 4 or more regular cups of coffee (equ. to approximately 400-500mg of caffeine). Moreover, the scientist found “a significant inverse association in all categories of prostate cancer except Gleason <7 grade” in both the “fixed-effects model” and the “random-effects model” (Lu. 2014).

    Wilson et al. also report an inverse association between coffee consumption and the incidence of highly malignant prostate cancer (Wilson. 2013). This means that drinking coffee is not only going to reduce your overall risk of developing prostate and other cancers (Geybels. 2013), it will also increase your chance that in the unfortunate case you still develop cancer, it’s going to be a benign and treatable form of prostate cancer.

  • Lignans (e.g. from flaxseed) – While many of you will probably know them as “bad anti-androgens”, there is little doubt that lignans from flax and other foodstuff inhibit cancer growth. What is particularly interesting about these agents is that they don’t work via the “regular” NF-kappaB pathway but inhibit the expression of the vascular endothelial growth favtor (VEGF; cf. Azrad. 2013).
  • Lycopene – It’s the bright red carotene and carotenoid pigment and phytochemical that gives tomatoes and other red fruits and vegetables, such as red carrots, watermelons, gac, and papayas, although not in strawberries, red bell peppers, or cherries their color.

    Based on the currently available evidence it appears to help not just with prostate, but also with pancreatic, intestinal and lung cancer (Giovannucci. 1999). In that, it makes a particularly effective adjunct to classic cancer therapy (Tang. 2011).

    Figure 2: Prostate cancer risk w/ high vs. low intakes of the given antioxidants according
    to XRCC1 genotype (Goodman. 2006)

    Unfortunately, the data is ambigious… as usual. Unlike for other agents, it does yet appear as if scientists have already identified a certain gene, i.e. XRCC1, which appears to determine whether you do or do not benefit from the consumption of increased amounts of tomato lycopene (Goodman. 2006).

    In view of the fact that certain genotypes actually increase their prostate cancer risk specifically if they are consuming both, a high amount of lycopene and vitamin E (alpha-tocopherol), the latest Cochrane Review on the protective effects of lycopene against prostate cancer considers the evidence for “preliminary” and “insufficient” (Ilic. 2011).

  • Fish oil / omega-3 – In spite of the fact that the media jumped at the finding of the SELECT trial (learn more) that claimed that selenium would be bad, while a high fish consumption or rather a high amount of omega-3s in the blood would protect you against prostate cancer, a close re-analysis of the data you can read up on at the website of the Life Extension Foundation indicates that this was all media hype.

    With a de facto difference of only 0.18% the difference was… well, you’d say a joke, scientists would say “within the margin of statistical error” and thus by no means significant. If you take an even closer look at the data, it would even seem as if omega-3 fatty acids would increase the risk of prostate cancer.

  • Resveratrol - If you look at the existing evidence you will be surprised to find studies that indicate that resveratrol increases (Klink. 2013) and studies that show that it inhibits prostate cancer growth (Iguchi. 2012; Kai. 2011).

    Again, it took a closer look at the data and another experiment to find out what really was going on: a dose-dependent effect with increased risk with low and decreased risk with high doses of resveratrol (Benitez. 2007). Bad news: With the current low biovailable oral resveratrol preparations you’re likely to end up in the “increased risk” resveratrol exposure zone.

  • Selenium – While I have mentioned it in the introduction already, it’s certainly worth taking a closer look at what selenium is actually supposed to do.

    In their 2011 review of the literature, Rizky Abdulah et al. didn’t just highlight the many different molecular pathways, by which selenium could protect you from developing cancer, they also point out that the type of selenium supplement used could be of critical importance with respect to the success of your efforts to avoid the development of cancer. In that,…

    In rodents selenium acts as corrosion inhibitor in the brain | learn more

    “[...] methylselenol is believed to be the critical metabolite in selenium chemoprevention. Since methylselenol is highly reactive, methylselenol precursors such as Semet and Se-mSC are important both in in vitro and in vivo experiments. Semet and Se-mSC conversion to methylselenol, however, requires enzymatic conversion by the enzyme β-lyase, which is 800 times less prevalent in human tissues than in mouse tissues.

    This may explain why the results of Semet and Se-mSC anticancer studies in humans were not as impressive as in vivo experiments. Although researchers have now turned to other Se compounds such as mSeA, which do not need enzymatic conversion to methylselenol, or selenite, which does not need to be converted to methylselenol for its anticancer properties, more substantial research on selenium compound metabolism in human tissues is necessary.” (Abdulah. 2011)

    In other words, as of now, we don’t know which form of selenium we actually have to use in human trials to generate similar impressive results as they have been observed in rodents.

    And as if that wasn’t already “bad” enough, a meta-analysis of intervention studies by Hurst et al. (2012) indicates that there is a very narrow “band” of serum concentrations, where selenium is actually good for you! When your selenium level passes 170 ng/ml the tumor-protective effect disappears and – worst case scenario – your risk increases. So remember: More does certainly not help more!

  • Silibin (from milk thistle) – You probably think of milk thistle as a “liver supplement”. In fact, its main active constituent will yet also reduce the efficacy of osteoclast cytokines and reduce the concentration of RANKL-ligands. Thus it will regulate the NF-κB und AP1 levels in cells and inhibit the proliferation, invasion and migration of metastatic prostate cancer (Ting. 2011; Chen. 2012) 
  • Vitamin D - Believe it or not: There are things vitamin D3 cannot do! One of this things is to protect you prostate cancer. That’s the prerogative of active vitamin D aka calciferol. In rodent studies and studies on human cell lines calciferol and multiple analogs of active vitamin D have shown to be promising drugs for prostate cancer protection, though (Tokar. 2005).
    Underestimated Vitamin D Sources: Eggs, Chicken, Pork, Fish & Dairy Contain Ready-Made 25OHD | more

    Since simply popping tons of vitamin D3 is (luckily) without effect on the levels of calciferol (otherwise you would run the risk of being calcified from the currently prevalent abuse of vitamin D3 supplements), using vitamin D3 is less effective, but not useless.

    In 2010, for example, Woo et al. observed that the time it took for the PSA levels of prostate cancer patients to double was significantly reduced, when the subjects received 2,000 IU of vitamin D3 per day (Woo. 2005) – an effect of which previous in vitro studies suggest that it could be due to the local conversion of D3 to active vitamin D in prostate cancer cells (Tokar. 2005).

  • Vitamin E - Needless to say that vitamin E has gotten a bad rep ever since scientists observed an increased risk when they gave the subjects of the SELECT trial vitamin E (learn more). Still, as long as you stay away from “classic” vitamin E and buy one of the still expensive tocotrienol supplements (or eat red palm oil), you can expect an anti-proliferative effect of the vitamins E (Conte. 2004; Srivastava. 2006)
It’s never too late to make a change! In September 2005, researchers from the University of California-San Francisco pub- lished a study that shows that intensive lifestyle changes (i.e. changin the way you eat, the amount of exercise you get, etc.) may affect the progression of prostate cancer in a highly beneficial way (Ornish. 2005) – with PSA reductions of -4%, reduced glucose levels (-70%!) improved blood lipids and higher, not lower testosterone levels.
Bottom line: While all of the above supplements and food constituents will help, nothing beats a healthy lifestyle with a balanced whole foods diet, stress control and regular exercise.

Overweight (+20% risk for BMI >25.38, already), gaining 5-10% weight after your 20s (+30%; Putnam. 2000), being self-employed (+170%) and thus probably stressed, having a family history of prostate cancer (father +140%, brother +420%), being a “former drinker” (beer +20%, wine +20%) or a current liquor drinker (+40%) and consuming more than 96g of alcohol per week (+50%), on the other hand, will – for most of the variables unnecessarily – increase your prostate cancer risk (Andersson. 1996) | Comment on FB!

References:

  • Abdulah, Rizky, et al. “Molecular targets of selenium in prostate cancer prevention (Review).” International journal of oncology 39.2 (2011): 301-309. 
  • Andersson, Swen-Olof, et al. “Lifestyle factors and prostate cancer risk: a case-control study in Sweden.” Cancer Epidemiology Biomarkers & Prevention 5.7 (1996): 509-513.
  • Azrad, Maria, et al. “Flaxseed-derived enterolactone is inversely associated with tumor cell proliferation in men with localized prostate cancer.” Journal of medicinal food 16.4 (2013): 357-360.
  • Benitez, Dixan A., et al. “Mechanisms Involved in Resveratrol‐Induced Apoptosis and Cell Cycle Arrest in Prostate Cancer—Derived Cell Lines.” Journal of andrology 28.2 (2007): 282-293. 
  • Chen, Rongxin, et al. “The significance of MMP-9 over MMP-2 in HCC invasiveness and recurrence of hepatocellular carcinoma after curative resection.” Annals of surgical oncology 19.3 (2012): 375-384.
  • Chiyomaru, Takeshi, et al. “Genistein up-regulates tumor suppressor microRNA-574-3p in prostate cancer.” PloS one 8.3 (2013): e58929. 
  • Conte, Carmela, et al. “γ‐Tocotrienol Metabolism and Antiproliferative Effect in Prostate Cancer Cells.” Annals of the New York Academy of Sciences 1031.1 (2004): 391-394.
  • Donald, J. L. “Plasma metabolic profiling reveals age-dependency of systemic effects of green tea polyphenols in mice with and without prostate cancer.” Molecular BioSystems 6.10 (2010): 1911-1916.
  • Geybels, Milan S., et al. “Coffee and tea consumption in relation to prostate cancer prognosis.” Cancer Causes & Control 24.11 (2013): 1947-1954. 
  • Giovannucci, Edward. “Tomatoes, tomato-based products, lycopene, and cancer: review of the epidemiologic literature.” Journal of the National Cancer Institute 91.4 (1999): 317-331.
  • Guo H, Xu YM, Ye ZQ, Yu JH, Hu XY. “Curcumin induces cell cycle arrest and apoptosis of prostate cancer cells by regulating the expression of IkappaBalpha, c-Jun and androgen receptor.” Pharmazie 68.6 (2013):431-4.
  • Hurst, Rachel, et al. “Selenium and prostate cancer: systematic review and meta-analysis.” The American journal of clinical nutrition 96.1 (2012): 111-122.
  • Iguchi, Kazuhiro, et al. “Antiandrogenic activity of resveratrol analogs in prostate cancer LNCaP cells.” Journal of andrology 33.6 (2012): 1208-1215. 
  • Joseph, Michael A., et al. “Cruciferous vegetables, genetic polymorphisms in glutathione S-transferases M1 and T1, and prostate cancer risk.” Nutrition and cancer 50.2 (2004): 206-213.
  • Kai, Li, and Anait S. Levenson. “Combination of resveratrol and antiandrogen flutamide has synergistic effect on androgen receptor inhibition in prostate cancer cells.” Anticancer research 31.10 (2011): 3323-3330.
  • Kirsh, Victoria A., et al. “Prospective study of fruit and vegetable intake and risk of prostate cancer.” Journal of the National Cancer Institute 99.15 (2007): 1200-1209.
  • Klink, Joseph C., et al. “Resveratrol worsens survival in SCID mice with prostate cancer xenografts in a cell‐line specific manner, through paradoxical effects on oncogenic pathways.” The Prostate 73.7 (2013): 754-762.
  • Kristal, Alan R., et al. “Baseline selenium status and effects of selenium and vitamin E supplementation on prostate cancer risk.” Journal of the National Cancer Institute 106.3 (2014): djt456.
  • Lu, Yu, et al. “Coffee consumption and prostate cancer risk: an updated meta-analysis.” Cancer Causes & Control 25.5 (2014): 591-604. 
  • Merkle, W. “Prostatakarzinomprophylaxe durch Nahrungsergänzungsmittel.” Der Urologe (2014): 1-7.
  • NCI (2013) Pomegranate: prostate cancer, nutrition and dietary supplements (PDQ). NCI, Bethesda. http://www.cancer.gov
  • Ornish, Dean, et al. “Intensive lifestyle changes may affect the progression of prostate cancer.” The Journal of urology 174.3 (2005): 1065-1070.
  • Pantuck, Allan J., et al. “Phase II study of pomegranate juice for men with rising prostate-specific antigen following surgery or radiation for prostate cancer.” Clinical Cancer Research 12.13 (2006): 4018-4026.
  • Putnam, Shannon D., et al. “Lifestyle and anthropometric risk factors for prostate cancer in a cohort of Iowa men.” Annals of epidemiology 10.6 (2000): 361-369.
  • Stenner-Liewen, Frank, et al. “Daily Pomegranate Intake Has No Impact on PSA Levels in Patients with Advanced Prostate Cancer-Results of a Phase IIb Randomized Controlled Trial.” Journal of Cancer 4.7 (2013): 597. 
  • Srivastava, Janmejai K., and Sanjay Gupta. “Tocotrienol-rich fraction of palm oil induces cell cycle arrest and apoptosis selectively in human prostate cancer cells.” Biochemical and biophysical research communications 346.2 (2006): 447-453.
  • Tang, Yaxiong, et al. “Lycopene enhances docetaxel’s effect in castration-resistant prostate cancer associated with insulin-like growth factor I receptor levels.” Neoplasia 13.2 (2011): 108-119. 
  • Ting, Harold, Gagan Deep, and Rajesh Agarwal. “Molecular mechanisms of silibinin-mediated cancer chemoprevention with major emphasis on prostate cancer.” The AAPS journal 15.3 (2013): 707-716. 
  • Tokar, Erik J., and Mukta M. Webber. “Chemoprevention of prostate cancer by cholecalciferol (vitamin D3): 25-hydroxylase (CYP27A1) in human prostate epithelial cells.” Clinical & experimental metastasis 22.3 (2005): 265-273.
  • Verhoeven, Dorette T., et al. “Epidemiological studies on brassica vegetables and cancer risk.” Cancer Epidemiology Biomarkers & Prevention 5.9 (1996): 733-748.
  • Wilson, Kathryn M., et al. “Coffee and risk of prostate cancer incidence and mortality in the Cancer of the Prostate in Sweden Study.” Cancer Causes & Control 24.8 (2013): 1575-1581.
  • Woo, Tony Choon Seng, et al. “Pilot study: potential role of vitamin D (cholecalciferol) in patients with PSA relapse after definitive therapy.” Nutrition and cancer 51.1 (2005): 32-36.

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The 16 Best Muscle-Building Tips On BodySpace!

Making your muscles grow takes proper training and nutrition, and often some sound advice. Ensure you're getting big and strong the right way with these 16 pro tips.

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Fructose as a Dieting Tool: 100g Fructose Per Day Exert Sign. Protein Sparing Effects & Ameliorate the Decline in Thyroid Hormones During Starvation Diet in the Obese

Fructose as an injectable Dieting Aid? Sounds crazy, but it works!

Would you ever have remotely considered that a high-fructose corn-syrup based sugar-sweetened beverage could help seven health obese women who are 35%-90% over their ideal weight lose weight? No, …?

Well, honestly, me neither and if we take a closer look at the experimental design of a 1986 study by Robert A. Gelfand and Robert S. Sherwin from the prestigious Yale University, we will have to relativize the aforementioned claim. Coke alone may not do the trick. Pure fructose, if it’s infused right into the bloodstream, on the other hand will “abolishes the entire hormone-substrate response to fasting, and spares body protein without raising insulin above postabsorptive levels.” (Gelfand. 1986)

Learn more about fructose at the SuppVersity

Bad Fructose not so Bad, After All! Learn its Benefits.

Fructose From Fruit is NOT the Problem

Americans Don’t Eat More Fructose These Days!

An Apple A Day, Keeps… & More (Guestpost)

Fructose is Not Worse Than Sugar

The Obesogenic Fructose Fat Connection

Before we are pondering the results, let’s first have a closer look at the actual design of a study was conducted to “examine the influence of low-dose fructose infusion on nitrogen economy and the metabolic response to fasting in man” (Gelfand. 1986 | I know that you should do that in “man”, not rodents, but that’s costly and has the aforementioned limitations).

To this ends, the aforementioned overweight to obese women who were not diabetic and normal blood glucose and insulin levels, had normal thyroid and liver function and had been consuming a weight maintenance diet with at least 200g of carbohydrates per day before they were recruited for the study, were fasted for a period of 10 days (they did get a multivitamin, a folic acid and a potassium chloride tablet to eat, though ;-) and randomly divided into 2 groups using a crossover design:

  • Group 1 (n = 4) received intravenous fructose during the last 3 days of the IO-day fasting period, while 
  • Group 2 (n = 3) received fructose for the initial 7 days of the fast 

In all subjects, fructose was administered by continuous intravenous infusion of a 10% solution in water (American McGaw), delivering 100 g of fructose (375 kcal) per day.

Figure 1: Changes in plasma glucose and insulin (left) and active thyroid hormone T3 (right) during the fast with and without fructose (Gelfand. 1986)

As you can see in Figure 1 the first thing the fructose did was to keep the blood sugar and insulin stable and the levels of the active thyroid hormone T3 (iodothyronine) from plummeting. In addition, the levels of the glycogen liberating hunger hormone glucagon remained stable over the course of the whole study period in the fructose arm(s) of the study, while it increased by more than 80% in the women who didn’t receive the fructose infusion.

Hormonal changes and real world effects!

Now hormonal changes are one thing. Real world effects which cannot always be predicted solely by endocrine parameters are yet often a whole different animal. I mean, who would have expected that the infusion of fructose and the previously described hormonal changes would be associated with an increased production of keton bodies (Blood beta-hydroxybutyrate; see Table 1)?

Table 1: Inhibitory Effect of Fructose on Starvation-Induced Ketosis. FFA Elevation,
Acidosis. and Hyperuricemia (Gelfand. 1986)

No one, well… what some of you may have expected are the decreases in bicarbonate and increases in uric acid, of which the latter have previously been reported to contribute to the metabolic derangements that occur with high fructose intakes on top of an already obesogenic diet (Sahebjami. 1971; Nakagawa. 2006).

Figure 2: Urinary ammonium loss with sodium bicarbonate (G2) or potassium + calcium carbonate (G3) vs. no buffer (G1) on a 93g all protein starvation diet (Gougeon-Reyburn. 1991)

Did you know that the addition of sodium bicarbonate or a combination of potassium bicarbonate and calcium carbonate can “buffer” the increased acidity that occurs on very low energy diets and minimize the urinary nitrogen loss in form of ammonia (see Figure 2)? No, well… I guess it’s about time you learn more about sodium bicarbonate, then ;-) It can, for example, also buffer the reduction in growth hormone production that occurs, when the acid level in your body is rising (see Figure 3 in previous article). Plus: It’s obviously a neat ergogenic.

Obviously, ketone bodies are nice, but certainly not the most relevant determinant of successful weight loss. Rather than that, a “reduced rate of energy expenditure” has long been touted as the main “risk factor for body-weight gain” (Ravussin. 1988) and thus unsuccessful dieting by scientists.

One of the factors that contributes to the “reduced rate of energy expenditure” is the the previously mentioned decline in thyroid hormone levels, of which you’ve just learned that it can be ameliorated by fructose injections (see Figure 1). Another one that is partly related to the decline in T3 is the loss of muscle mass – a process of which Byerley et al. (1996) argue showed that it does not have the protein sparing effects many people believe it would have.

Figure 3: Fructose decreases the total urinary nitrogen loss by ~40% (Gelfand. 1986).

In view of the results of Byerley & Heber’s human study that investigated the metabolic effects of triiodothyronine replacement during fasting in obese subjects and found no effects when the protein intake was >70g/day (or 50g were complemented by 76g carbohydrates), it is thus much less surprising that the provision of fructose increased the triiodothyronine levels and decreased theh net urinary protein loss. A brief look at the serum amino acid levels of the subjects (not shown in Figure 3) suggests that fructose may have had a BCAA sparing effect, as well.

Bad Fructose? Increased Glycogen Synthesis, Reduced Glycemia, Higher Glucose Oxidation – When Do These Beneficial Effects Occur? And Why Don’t They Prevail? | Read more!

Bottom line: Overall, it is unquestionably remarkable how effectively less than 375kcal of energy from fructose can reverse major components of the starvation response in human beings, i.e. abolishes the entire hormone-substrate response (specifically the decline in T3), spare body protein, and reduce urinary mineral (specifically sodium) loss.

Unfortunately, one very important question remains: What will happen if the fructose has to pass by the liver first, i.e. if it is ingested orally, not injected? 

The absence of corresponding research and the question, whether the same effects will be observed if small amounts of fructose are added to a saner form of “crash dieting”, e.g. a protein modified fast, make the results of the study at hand interesting, but difficult to interpret.

References:

  • Byerley, L. O., and D. Heber. “Metabolic effects of triiodothyronine replacement during fasting in obese subjects.” The Journal of Clinical Endocrinology & Metabolism 81.3 (1996): 968-976. 
  • Gelfand, Robert A., and Robert S. Sherwin. “Nitrogen conservation in starvation revisited: Protein sparing with intravenous fructose.” Metabolism 35.1 (1986): 37-44.
  • Gougeon-Reyburn, Réjeanne, François Larivière, And Errol B. Marliss. “Effects Of Bicarbonate Supplementation On Urinary Mineral Excretion During Very Low Energy Diets.” The American Journal Of The Medical Sciences 302.2 (1991): 67-74.
  • Nakagawa, Takahiko, et al. “A causal role for uric acid in fructose-induced metabolic syndrome.” American Journal of Physiology-Renal Physiology 290.3 (2006): F625-F631.
  • Ravussin, Eric, et al. “Reduced rate of energy expenditure as a risk factor for body-weight gain.” New England Journal of Medicine 318.8 (1988): 467-472.
  • Sahebjami, Hamid, and Raymond Scalettar. “Effects of fructose infusion on lactate and uric acid metabolism.” The Lancet 297.7695 (1971): 366-369.

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Avoid These 5 Weight-Loss Pitfalls!

Dropping body fat isn't as easy as just working out and eating right. Misinformation can quickly lead to slip-ups and pitfalls. Avoid them with these 5 tips!

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