Cheese & Your Health: CVD, Cancer & Metabolic Syndrome - Cheesy Science or Scientific Revelation? A Brief Review

Cheese & Your Health: CVD, Cancer & Metabolic Syndrome - Cheesy Science or Scientific Revelation? A Brief Review

cheese dairy diet health healthy diet healthy eating lose fat

Cheeses come in all forms and colors.

Cheese is not exactly the first food that comes to mind when we think about "healthy eating". Rightly so? Today's overview of recent cheese studies tries to answer this question.

The article will, among other things, also address the claim that cheese was addictive (see red box) and / or that the consumption of a dairy product with a saturated fat content that is second only to that of butter would harm your cardiovascular and metabolic health.

So, where do we start? Netherlands? Well, even though the Dutch are famous for the many different types of cheese they produce and consume, they are probably not the ones who "invented" it. Rather than that it appears to be certain that the first cheeses were produced 5,000 BC - accidentally.

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Back in the day, humans had not invented pottery and thus stored their foods - including their milk - in animal stomachs, ... stomachs the cuagulating enzyme content of which turned milk into curd during storage (Fox. 1993). The first recorded "production" of cheese, in that case Gorgonzola dates back to the year 897, however (see Table 1).

Table 1: First Recorded Date for some Major Cheese Varieties (Fox. 1993).

Another cheesy fact about the Netherlands is that the Dutch would be the world's #1 cheese producer and consumer. Both is not the case! Rather than that, France holds both the title of the greatest producer (1.3 m tonnes) and consumer (22kg / per capita | Fox. 1993 // relative to their total dairy consumption, the Italians are the kings of cheese w/ up to 28% and 33%  of the dairy intake from cheese of women and men in the province Ragusa | Hjartåker. 2002). It is thus also France, where we will probably find the most significant evidence with regards to the health effects of cheese consumption. The most prominent study investigating this issue comes from the Aarhus University (Zheng. 2015)..

Is cheese the reason for the "French paradox"?

In said study, Zheng et al. used an NMR-based metabolomics approach "to investigate the differentiation between subjects consuming cheese or milk and to elucidate the potential link to an effect on blood cholesterol level" (Zheng. 2015). To this ends, the researchers recruited fifteen healthy young men for a full crossover study during which all subjects consumed three isocaloric diets with similar fat contents that were either (1) high in milk, (2) high in cheese or (3) contained only limited amounts of dairy for 14 days.

Only the fat "Norvegia" gouda has cholesterol-lowering effects in an 8 week RCT (Nilsen. 2015).

Question 1 - Does the type of cheese matter? High fat may matter. Well, "fake cheese" that's made from vegetable oils + tons of additives, as you will find it on most frozen Pizza from the supermarket is obviously not an option, but even among "real" cheeses there appear to be differences in terms of their individual health effects. The results of a 2015 study from Norway, for example, show that only fat gouda (80g/day), yet not fat- and salt-free Gamalost, a traditional form of Norwegian cheese will significantly reduce elevated cholesterol levels in non-medicated men and women over 18 years of age (Nilsen. 2015).

As the data from the scientists urine and feces analyses shows, the cheese diet significantly reduced the urinary citrate, creatine, and creatinine levels and significantly increased the microbiota-related metabolites butyrate, hippurate, and malonate compared to the milk diet. Overall, the study shows...

"[...] that cheese consumption is associated with an increased level of SCFAs in the gut, possibly induced by stimulation of beneficial gut microbiota, as well as an increased extent of lipid excretion with resultant beneficial effects on cholesterol metabolism"(Zheng. 2015 | my emphasis).

In conjunction with the significant reduction of the subjects' TMAO production [Trimethylamine N-oxide has been associated with increased CVD and even cancer risk] of which the authors rightly say that it could "also contribute to potential beneficial effects of cheese intake on the risk of CVD" (Zheng. 2015), the results of this controlled human trial are in stark contrast to the cheese = "high cholesterol" = "bad for your heart" myth that's still so prevalent:

"Overall, this metabolomics study suggests that cheese could be an important piece in the French paradox puzzle. However, further studies are needed to explore the exact metabolic mechanisms linking cheese consumption, stimulation of the gut microflora, and cholesterol metabolism" (Zheng. 2015 | my emphasis)

Just as many other researchers working in this area, Zheng et al. received support for their study from the dairy industry - a factor that is as prevalent in other areas of nutrition research, but interestingly most heavily criticized for dairy (Armstrong. 2005) and, obviously, artificial sweeteners.

Percentages of women reporting a craving for a given food at four different timepoints during their menstrual cycle (Rodin. 1991). 

Question 2 - Is cheese addictive? Prolly not! Even though the whole concept of food addiction is still contested (Rogers. 2000; Corwin. 2009; Albay-rak. 2012; Ziauddeen. 2012; Hebebrand. 2014), the Internet is full of "information" about the addictive nature of cheese. Claims that are not really backed up by science, as the data from Judith Rodin et al.'s study of the food cravings of women during different phases of the menstrual cycle in the Figure (left) shows (Rodin. 1991) - the real world does thus not confirm the relevance of the theor. addictive potential of casomorphines (Freye. 2004).

In general, rather than a role for individual molecules, the existing data appears to suggest "addictive", or rather hyperpalatable foods share common macronutrient compositions that distinguish a dairy queen chocolate ice cream cone with 34 g sugar 10 g fat and 160 mg sodium (+22 extra ingredients) per serving from roasted chicken breast or an apple (Gearhardt. 2011). This does not exclude that you can be "addicted" to cheese, but the same goes for carrots of which Kaplan reported 10 years ago that they got a 49-year-old woman addicted (Kaplan. 1996).

The reasons why I would argue that you can still put faith into the accuracy of the results Zheng et al. present in their paper are: (1) they openly declared the funding, i.e. support by The Danish Council for Strategic Research, Arla Foods, and the Danish Dairy Research Foundation in the project “FIAF - Milk in regulating lipid metabolism and overweight. Uncovering milk’s ability to increase expression and activity of fasting-induced adipose factor” (10-093539) and (2) the supporting evidence from various previous studies:

• Beneficial effect on CVD health - "The majority of prospective studies and meta-analyses examining the relationship between milk and dairy product consumption and risk of CVD show that milk and dairy products, excluding butter, are not associated with detrimental effects on CVD mortality or risk biomarkers that include serum LDL-cholesterol" (Lovegrove. 2016).
  

  

  Figure 1: Unlike 40 g dairy fat from butter, 40g of fat from matured cheddar cheese do not sign. affect the levels of total cholesterol and LDL in a 4 weeks cross-over study in healthy subjects (Nestel. 2005).

  With the latest evidence for this claim coming from an impartial source, namely Iran, where Sadeghi et al. found that higher cheese intakes are are associated with 19% reduced risk of metabolic syndrome and 13% reduced risk of suffering from (too) low HDL-C level, one may still doubt the objectivity of this claim being made at a conference about animal products, but can hardly argue that there was only potentially biased research to support Lovegrove's claim and the conclusions of the latest meta-analysis of its effects on blood lipids (de Goede. 2015):

  "Compared with butter intake, cheese intake (weighted mean difference: 145.0 g/d) reduced low-density lipoprotein cholesterol (LDL-C) by 6.5% (−0.22 mmol/l; 95%CI: −0.29 to −0.14) and high-density lipoprotein cholesterol (HDL-C) by 3.9% (−0.05 mmol/l; 95%CI: −0.09 to −0.02) but had no effect on triglycerides" (de Goede. 2015).

  In addition every regular gouda (and many other classic cheeses) contains peptides that have proven to have anti-hypertensive effects (Saito. 2000) and will thus lower the #1 risk factor for stroke and related cardiovascular problems - including death (Fagard. 2008).
• Reduced breast cancer risk -  A case-control study from the Netherlands suggests that each 60g increase in gouda intake will reduce the breast cancer risk of 25-64 year-old women (analysed according to age groups) with a 34% reduced risk of breast cancer.
  

  

  Figure 2 A high intake of gouda is associated with highly significant reductions in breast cancer risk even after adjusting for familial history, smoking,education, contraceptive use, age at menarche and first full-term pregnancy, parity, body mass index, and geographic area in Dutch women (van't Veer. 1989)

  What is also interesting about the effects plotted in Figure 2 is that a similar beneficial effect was not observed for milk (had no negative effect, either) or similarly low intakes of other fermented dairy (van't Veer).
• Anti-NAFLD and prometabolic effects - At least in comparison to a butter-fat based diet a similarly low fat (20%) likewise AIN76 (that's std. rodent chow) based diet with freeze-dried cheese powder significantly reduced the accumulation of triglyceride and cholesterol in the liver (P = 0.016 and P < 0.001, respectively) of rats who received the cheese or control diet in a 9-week study.
  

  

  Figure 2: Liver triglyceride (a) and total cholesterol (b) concentrations in rats fed control or cheese diet. Mean ± standard error. Asterisks indicate significant differences between groups (Higurashi. 2016)

  Just like the previously reported human studies, the rodent study als found significant increases in HDL and decreases in non-high-density lipoprotein (non-HDL) cholesterol, as well as elevated levels of metabolically healthy serum adiponectin concentration at week 9 in rats fed the cheese diet. To which degree this effect was due to or related to the increase in fat excretion in the feces will have to be determined in future studies. What appears to be clear, though, is that these "results suggest that cheese mediates various beneficial effects for preventing the development of metabolic syndrome by suppressing the accumulation of fat in the liver" (Higurashi. 2016).
• High nutritional value - Cheese is a low carbohydrate food that's packed with high concentration of essential amino acids saturated fats that could be good, not bad for your health (e.g. conjugated linoleic acid and sphingolipids present in cheese may have anti-carcinogenic properties, too), a lot of highly bioavailable calcium with beneficial effects on bone, teeth, blood pressure and weight loss (when combined with low-energy diets). Reason enough for researchers to state that "[c]heese is an important dairy product and an integral part of a healthful diet due to its substantial contribution to human health" (Walther. 2008).

Whether the average young, whites, female knows all the above or whether there's another reason that this part of US society consumes the highest amounts of cheese (Glanz. 1998) is something I cannot tell you. What I can tell you, though, is that the previously presented evidence suggests that weight concerns should not, as they still were in 1998 in the US (Glanz. 1998), be a reason for you not to consume cheese (in controlled amounts). Rather than that you should follow the example of the rich and intelligent of which a more recent study shows that they tend to consume the most cheese in Europe (Sanchez-Villegas. 2003).

A high cheese will also increase the level of the "good lipoproteins" HDL and apo A-I (Thorning. 2015a).

Bottom line: Don't get me wrong. The purpose of today's article is not to promote a "cheese only diet" or to tell you to consume at least X amounts of cheese per day. It is rather meant to critically evaluate the irrational fear that still characterizes the relationship of many health-conscious dieters to (esp. fatty) cheeses.

When consumed in moderation, cheese is not just a highly nutritious food, but can, as a lot of the more recent studies indicate, even have beneficial effects on your cardiovascular and metabolic health that are probably mediated by key nutrients and the beneficial effect cheese will have on your microbiome | Comment!

References:

• Albayrak, Ö., Sebastian Mathias Wölfle, and Johannes Hebebrand. "Does food addiction exist? A phenomenological discussion based on the psychiatric classification of substance-related disorders and addiction." Obesity facts 5.2 (2012): 165-179.
• Corwin, Rebecca L., and Patricia S. Grigson. "Symposium overview—food addiction: fact or fiction?." The Journal of nutrition 139.3 (2009): 617-619.
• de Goede, Janette, et al. "Effect of cheese consumption on blood lipids: a systematic review and meta-analysis of randomized controlled trials." Nutrition reviews 73.5 (2015): 259-275.
• Fagard, Robert H., et al. "Daytime and nighttime blood pressure as predictors of death and cause-specific cardiovascular events in hypertension." Hypertension 51.1 (2008): 55-61.
• Fox, P. F. "Cheese: an overview." Cheese: chemistry, physics and microbiology. Springer US, 1993. 1-36.
• Freye, Enno. "Exorphine (exogene Opioidpeptide) und β-Casomorphine." Opioide in der Medizin. Springer Berlin Heidelberg, 2004. 323-324.
• Gearhardt, Ashley N., et al. "Can food be addictive? Public health and policy implications." Addiction 106.7 (2011): 1208-1212.
• Glanz, Karen, et al. "Why Americans eat what they do: taste, nutrition, cost, convenience, and weight control concerns as influences on food consumption." Journal of the American Dietetic Association 98.10 (1998): 1118-1126.
• Hebebrand, Johannes, et al. "“Eating addiction”, rather than “food addiction”, better captures addictive-like eating behavior." Neuroscience & Biobehavioral Reviews 47 (2014): 295-306.
• Higurashi, Satoshi, et al. "Cheese consumption prevents fat accumulation in the liver and improves serum lipid parameters in rats fed a high-fat diet." Dairy Science & Technology (2016): 1-11.
• Hjartåker, A., et al. "Consumption of dairy products in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort: data from 35955 24-hour dietary recalls in 10 European countries." Public health nutrition 5.6b (2002): 1259-1271.
• Lovegrove, Julie A., and Ditte A. Hobbs. "Plenary Lecture 2: Milk and dairy produce and CVD: new perspectives on dairy and cardiovascular health." Proceedings of the Nutrition Society (2016): 1-12.
• Nestel, P. J., A. Chronopulos, and M. Cehun. "Dairy fat in cheese raises LDL cholesterol less than that in butter in mildly hypercholesterolaemic subjects." European journal of clinical nutrition 59.9 (2005): 1059-1063.
• Nilsen, Rita, et al. "Effect of a high intake of cheese on cholesterol and metabolic syndrome: results of a randomized trial." Food & nutrition research 59 (2015).
• Rodin, Judith, et al. "Food cravings in relation to body mass index, restraint and estradiol levels: a repeated measures study in healthy women." Appetite 17.3 (1991): 177-185.
• Rogers, Peter J., and Hendrik J. Smit. "Food craving and food “addiction”: a critical review of the evidence from a biopsychosocial perspective." Pharmacology Biochemistry and Behavior 66.1 (2000): 3-14.
• Saito, T., et al. "Isolation and structural analysis of antihypertensive peptides that exist naturally in Gouda cheese." Journal of Dairy Science 83.7 (2000): 1434-1440.
• Sanchez-Villegas, A., et al. "A systematic review of socioeconomic differences in food habits in Europe: consumption of cheese and milk." European journal of clinical nutrition 57.8 (2003): 917-929.
• Thorning, Tanja K., et al. "Diets with high-fat cheese, high-fat meat, or carbohydrate on cardiovascular risk markers in overweight postmenopausal women: a randomized crossover trial." The American journal of clinical nutrition 102.3 (2015): 573-581.
• Thorning, Tanja K., et al. "Cheddar Cheese Ripening Affects Plasma Nonesterified Fatty Acid and Serum Insulin Concentrations in Growing Pigs." The Journal of nutrition 145.7 (2015b): 1453-1458.
• van't Veer, Pieter, et al. "Consumption of fermented milk products and breast cancer: a case-control study in The Netherlands." Cancer research 49.14 (1989): 4020-4023.
• Zheng, Hong, et al. "Metabolomics investigation to shed light on cheese as a possible piece in the French paradox puzzle." Journal of agricultural and food chemistry 63.10 (2015): 2830-2839.
• Ziauddeen, Hisham, I. Sadaf Farooqi, and Paul C. Fletcher. "Food addiction: is there a baby in the bathwater?." Nature Reviews Neuroscience 13.7 (2012): 514.

Taurine Boosts Good Gut Bacteria & Short-Chain Fatty Acid Prod. | 1st Study to Show Natural Beats Synthetic Taurine

Taurine Boosts Good Gut Bacteria & Short-Chain Fatty Acid Prod. | 1st Study to Show Natural Beats Synthetic Taurine

bacteria bacteriodetes bad bacteria firmicutes good bacteria health helicobacter microbiome natural taurine SCFA short-chain fatty acids synthetic taurine synthetic vitamins taurine

The bacteria in our guts are the latest rage in medical sciences... and taurine, especially natural taurine, may be a way to modulate them in beneficial ways.

It has been some time since the last taurine article on the SuppVersity (read all articles). There was simply a lack of interesting studies... until now, or rather until the latest study of scientists from the Zhejiang University of Technology which suggests that taurine "might be of benefit to health by inhibiting the growth of harmful bacteria, accelerating the production of SCFA and reducing LPS concentration" (Yu. 2016).

As the authors of the paper point out, taurine is a necessary amino acid that taurine plays an important role in the regulation of neuroendocrine functions and nutrition.

In previous studies, taurine was shown to improve immunity, resist oxidation, delay senility, reduce blood pressure, promote recovery from acute hepatitis, etc. (Averin. 2015; Wang. 2013; De Luca. 2015; Ito. 2012). In addition, taurine can also improve the metabolism of the nutrients and play an important role in the regulation of neuroendocrine (Cuttitta et al. 2013; Camargo et al. 2015).

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With their latest study, the Chinese scientists Haining Yu, Zhengzhao Guo, Shengrong Shen , an Weiguang Shan were now able to add yet another beneficial health effect of taurine to the previous, impressive list: taurine's effect on gut microbes and metabolism.

Food	Amount	Taurine (mg)
Cheese	3 ounces	1000
Cheese,cottage	1 cup	1700
Milk,whole	1 cup	400
Yogurt	1 cup	400
Wild game	3 ounces	600
Pork	3 ounces	540
Granola	1 cup	650
Oatmeal flakes	1 cup	500
Chocolate	1 cup	400
Meat (luncheon)	1 cup	390
Wheat germ,toasted	1/4 cup	350
Egg	1 (medium size)	350
Turkey	3 ounces	240
Duck	3 ounces	240
Chicken	3 ounces	185
Sausage	3 ounces	185
Avocado	1/2 (medium)	75
Table 1: It doesn't always have to be supplements - Taurine content of selected foods (USDA Handbook #8)

As you'd expect it for a "first of its kind" study, the researchers used a rodent model to evaluate the effects of a human equivalent dose of ~1g of taurine in BALB/C who were randomly divided into three experimental groups:

• the first group was administered saline (CK),
• the second group was administered 165 mg/kg natural taurine (NE) and
• the third group one administered 165 mg/kg synthetic taurine (CS).

With the NE and CS group, this is also one of the few studies to distinguish between "natural" and "synthetic" taurine, which is obtained from isethionic acid (2-hydroxyethanesulfonic acid) and not extracted from animal bile, usually that of the ox, and subjected to a series of purification procedures by several different methods (Gioacchini. 1995).

Figure 1: Effects of taurine on gut bacteria abundance (Yu. 2016).

To assess the effects, the gut microbiota composition in mice feces was analyzed by metagenomics technology, and the content of short-chain fatty acids (SCFA) in mice feces was detected by gas chromatography (GC), while the concentrations of lipopolysaccharide (LPS) and superoxide dismutase (SOD) were detected by a LPS ELISA kit and a SOD assay kit, respectively.

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Is "natural taurine" the "better taurine"? In the study at hand, it seems as if this was the case. The only evidence from other studies that suggests that the source of taurine matters, however, is 1995 paper by Gioacchini et al. who developed a method to distinguish the two and may thus have a vested interest in stating that "[n]atural taurine is an essential constituent of formula milk for infants and, because of the inferior nutritional value (δ), of synthetic forms, it is important to discriminate between these and taurines derived from a natural source" (Gioacchini. 1995). Another study shows that the allergy risk for synthetic taurine appears to be elevated (Lee. 2013).

Why this is the case or what triggers any differences in the effect on the microbiome is something I cannot tell you: if the molecules were structurally different, Gioacchini et al. would after all not have had to use the 13C/12C ratio that is also used to date bones and other relicts. It could eventually be solely a question of dosage - with "inferior nutritional value" the synthetic taurine may have to be dosed much higher... as high as in most previously published human studies which generated the most impressive results with 3-6g and thus 3-6x more taurine per day than the human equivalent dose (learn more about the HED concept) of the study at hand.

As the data in Figure 1 indicates, taurine had profound effects on gut microbiota could reduce the abundance of Proteobacteria, especially Helicobacter (see Figure 1, bottom right). In that, it is interesting to see that the natural taurine ...

• had more pronounced beneficial effects on the count of good bacteroidetes and was more potent than the synthetic version when it comes to reducing proteobacteria and helicobacter, and even more intriguingly
• had opposite effects on firmicutes which make up the largest portion of the mouse and human gut microbiome, can't be described as "beneficial" or "bad" as a whole, but have been shown to be involved in energy resorption and obesity

In line with the last-mentioned increase in firmicutes is the scientists' observation that the SCFA content was increased in feces of the NE group, but not the CS group that received the synthetic taurine supplement.

Figure 2: Short-chain fatty acid (SCFA) and Activity of superoxide dismutase (SOD) levels in response to natural (NE), synthetic taurine (CS) and saline control (CK) supplementation in mice (Yu. 2016).

That's interesting, also because this change went hand in hand with a 'natural exclusive' LPS content was decreased, but similar increases in the activity of the antioxidant SOD enzyme in serum and livers of the both taurine groups.

None of the previous taurine studies declared whether the chemical they used was "natural" or "synthetic", I thus suspect that a synthetic version was used in most if not all of them - that this could make a difference is still both surprising and intriguing.

Bottom line: While it is correct that both "natural taurine and the synthetic taurine could regulate the gut micro-ecology, which might be of benefit to health by inhibiting the growth of harmful bacteria" (Yu. 2016), it is quite intriguing that only the natural taurine accelerated the production of SCFA and reducing LPS concentration, while the synthetic taurine did not.

Unfortunately, I have no studies to tell you if there's (a) a general advantage of natural over synthetic taurine (see red box, too), or (b) whether your taurine is natural or synthetic. If the previous quote (see red box) from Gioacchini et al. is accurate, though, it would appear that (a) 'natural' was superior and that (b) your taurine supplement was almost certainly nor extracted from ox-bile or another expensive natural source | Comment on Facebook!

References:

• De Luca, Annamaria, Sabata Pierno, and Diana Conte Camerino. "Taurine: the appeal of a safe amino acid for skeletal muscle disorders." Journal of translational medicine 13.1 (2015): 1.
• Gioacchini, Anna Maria, et al. "Differentiation between natural and synthetic taurine using the 13C/12C isotope ratio." Rapid communications in mass spectrometry 9.12 (1995): 1106-1108.
• Ito, Takashi, Stephen W. Schaffer, and Junichi Azuma. "The potential usefulness of taurine on diabetes mellitus and its complications." Amino acids 42.5 (2012): 1529-1539.
• Lee, Seung-Eun, et al. "A case of taurine-containing drink induced anaphylaxis." Asia Pacific Allergy 3.1 (2013): 70.
• Yu, Haining, et al. "Effects of taurine on gut microbiota and metabolism in mice." Amino acids (2016): 1-17.

The 'Wim Hof Method' - Effective? What Science Can Tell Us

The 'Wim Hof Method' - Effective? What Science Can Tell Us

anti-inflammatory destress health immune health immune system inflammation stress the hof method wim hof wim hof method

If someone markets his program the way Hof does, i.e. as a means to "Become A 'Super' Version Of Yourself In Just 10 Short, Life Transforming Weeks" (WimHofMethod.com), you should rightly be skeptical.

You know that I am no fan of "works for me (N=1), so buy my e-book"-approaches. Until recently, the so-called "Wim Hof Method" was yet exactly that: an N=1 (+ dubious X) approach to health and performance enhancement... and yes, that is "until recently", or rather "until two years ago", because two years ago, Matthijs Kox and colleagues from the Nijmegen Institute for Infection, Inflammation and Immunity, the Radboud University (will wonders never cease) the Yale University School of Medicine (Kox. 2014) published a study with the not so telling title "Voluntary activation of the sympathetic nervous system and attenuation of the innate immune response in humans" in the peer-reviewed scientific journal PNAS.

The study used a parallel randomized controlled design and was registered at ClinicalTrials.gov as NCT01835457. After approval by the local ethics committee of the Radboud University Nijmegen Medical Centre (CMO 2012/455), 30 healthy, nonsmoking, Dutch male volunteers were included in the trial.

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Exclusion criteria were: febrile illness during the 2 wk before the endotoxemia experiment, taking any prescription medication, history of spontaneous vagal collapse, practicing or experience with any kind of meditation, or participation in a previous trial where LPS was administered.

Table 1: Subject demographic characteristics (Kox. 2014).

The subjects were randomly allocated to the trained group (n = 18) or the control group (n = 12) by the opening of a sealed envelope prepared by a research nurse not involved in the study. After having fulfilled the training program, 12 of the 18 trained subjects were randomly assigned to participate in the experimental endotoxemia experiments (see Figure 1).

The study itself (which excluded several of the originally 30 subjects, because their reaction to endotoxemia, i.e. the influx of  (potentially) pathogenic metabolic byproducts of bacteria into their blood was "odd" (i.e. too extreme as in too low or too high) was sequentially conducted in two identical blocks, each consisting of nine subjects in the trained group (of which six finally participated in the endotoxemia experiments) and six subjects in the control group. As the authors point out,

"[...t]his design was chosen to minimize the bias due to differences in the interval between the end of the training period and the endotoxemia experiments. As the aim of [their] study was to investigate the effects of the training intervention on the innate immune response in a standardized model of systemic inflammation, [they] did not assess the effects of the training intervention on immune system parameters in the absence of endotoxemia" (Kox. 2014). 

A schematic overview of the study design (one block) is depicted in Fig. S3. The trained group was trained by Dutch individual Wim Hof and three trainers who previously received an instructor course by Wim Hof to become a trainer. A medical doctor of the study team (L.T.v.E.) and the principal investigator (M.K.) were present during all training sessions (in Poland and in The Netherlands), and during the experimental endotoxemia experiments. The first 4 d of the training program took place in Poland and were most intensive.

The Internet is full of praise for Hof's method, but that's not scientific eviden-ce (infographic from therenegade-pharmacist.com)... it does show that Hof is a good marketer, though ;-)

What did the program look like? The program consisted of three main elements: meditation, exposure to cold, and breathing techniques. (i) Meditation: so-called “third eye meditation,” a form of meditation including visualizations aimed at total relaxation. (ii) Voluntary cold expo-sure: standing in the snow barefoot for up to 30 min and lying bare chested in the snow for 20 min; daily dipping / swimming in ice-cold water (0–1 °C) for up to several minutes (including complete submersions); and hiking up a snowy mountain (elevation: 1,590 m) bare chested, wearing nothing but shorts and shoes at temperatures ranging from −5 to −12 °C (wind chill: −12 to −27 °C).

(iii) Breathing techniques, consisting of two exercises: in the first exercise subjects were asked to hyperventilate for an average of 30 breaths. Subsequently, the subjects exhaled and held their breath for ∼2–3 min (“retention phase”). The duration of breath retention was entirely at the discretion of the subject himself. Breath retention was followed by a deep inhalation breath, that was held for 10 s. Subsequently a new cycle of hyper/hypoventilation began. The second exercise consisted of deep inhalations and exhalations in which every inhalation and exhalation was followed by breath holding for 10 s, during which the subject tightened all his body muscles. These two breathing exercises were also performed during the endotoxemia experiments. Additional element of the training program consisted of strength exercises (e.g., push-ups and yoga balance techniques).

After returning from Poland, the subjects practiced the techniques they learned daily by themselves at home (2–3 h/d; cold exposure was achieved through taking cold showers) until the endotoxemia experiment day (5–9 d later).

Figure 1: Study design. This block was carried out twice in identical fashion, resulting in 12 subjects in both groups that underwent experimental endotoxemia. CT, control subject; TR, trained subject (Kox. 2014).

After training the method at home, all subjects returned to the lab, where a final group training took place and at the end of this day, six of the nine trained subjects (in each block) were randomly selected for participation in the endotoxemia experiments, using the sealed envelope method. Then, ...

"[...t]he selected subjects practiced in a final training session led by Wim Hof on the day before the endotoxemia experiment day. Wim Hof was present to coach the subjects during the endotoxemia experiment days during the 3 h that the subjects in the trained group practiced the learned techniques. The control group did not undergo any training procedures throughout the study period" (Kox. 2014).

To evaluate the effect of Hof's method on the subjects' immune system, the subjects, who had refrained from caffeine- or alcohol-containing substances 24 h before the start of the experiment, and food 10 h before the start of the endotoxemia experiment, were injected purified lipopolysaccharides from Escherichia coli, which were supplied as a lyophilized powder that was reconstituted in 5 mL saline 0.9% for injection and vortex mixed for at least 20 min after reconstitution.

Figure 2: Cardiorespiratory parameters, temperature, and symptoms (A-I), as well as plasma
cathecholamine concentrations and serum cortisol concentrations during experimental endotoxemia
in control (dotted line) and trained (solid line) subjects (J-M | Kox. 2014).

As the scientists point out, "[t]he LPS solution was administered as an i.v. bolus injection at a dose of 2 ng/kg body weight in 1 min at T = 0 h (Kox. 2014). More specifically, ...

"[...a] cannula was placed in an antecubital vein to permit infusion of 0.9% NaCl solution; the subjects received 1.5 L 0.9% NaCl during 1 h starting 1 h before endotoxin infusion (prehydration) as part of our standard endotoxemia protocol (29), followed by 150 mL/h until 6 h after endotoxin infusion and 75 mL/h until the end of the experiment" (Kox. 2016).

To estimate the effect of the breathing techniques, the authors measured not just cardiorespiratory parameters, temperature, and symptoms, but also the levels of catecholamines, cortisol and plasma cytokines (stress), as well as the leukocyte count (immune reaction) and conducted correlation analyses of all these variables.

Figure 3: Plasma cytokine concentrations during endotoxemia in control and trained subjects. (A, C, E, and G) Median values of pro- (TNF-α, IL-6, and IL-8) and anti-inflammatory (IL-10) cytokines (n = 12 per group). (B, D, F, and H) Median ± interquartile range of area under curve (AUC) of pro- (TNF-α, IL-6, and IL-8) and anti-inflammatory (IL-10) cytokines (n = 12 per group; unit: ×104 pg/mL·h). P values were calculated using Mann–Whitney u tests (Kox. 2014).

The results are - initially (eventually, it's a normal stress response, see Bottom Line)- quite astonishing, as the "intervention group, practicing the learned techniques" (Kox. 2014) didn't just show symptoms of being suffocated, i.e. am intermittent respiratory alkalosis and hypoxia resulting and corresponding increases in the levels of the stress hormones epinephrine in the blood, but also ...

• 

  Figure 3: Correlation analysis (Kox. 2014).

  significant increases of the anti-inflammatory cytokine IL-10, which correlated strongly with the preceding increase in epinephrine levels (see Figure 3A), as well as
• significant reductions of the proinflammatory mediators TNF-α, IL-6, and IL-8, which, in turn, correlated negatively with IL-10 levels.

In conjunction with the significant reduction of "flu-like symptoms", the scientists observed in the intervention group, the study at had does therefore in fact "demonstrate that voluntary activation of the sympathetic nervous system results in epinephrine release and subsequent suppression of the innate immune response in humans in vivo" (Kox. 2015).

Wow! This really works!? Yes, the study at hand confirms that the long-held theory that both, the autonomic nervous system and innate immune system, cannot be voluntarily influenced must be considered disproven - the "Wim Hof Method", of which the authors of the present paper highlight that it consists of techniques that can be "learned in a short-term training program" (Kox. 2014) seems to do what scientists have long considered impossible: it allows people like you and me to directly influence their sympathetic nervous system and immune system in a way that triggers highly pronounced increases in the stress hormone epinephrine and down-stream immune effects in form of increases of the production of anti-inflammatory mediators and a subsequent dampening of the proinflammatory cytokine response to an (albeit artificial) immune challenge with bacterial endotoxin.

Believe it or not, but an intense workout will have pretty much the same effects on inflammation (in this case triggered by the workout itself) as the "unique" Hof Method (figure from Petersen. 2005; expanded). A study that evaluates the conditioning effect in the same endotoxin model has yet, as far as I know, still to be done.

As Kox et al. point out, their study "could have important implications for the treatment of a variety of conditions associated with excessive or persistent inflammation, especially autoimmune diseases in which therapies that antagonize proinflammatory cytokines have shown great benefit" (Kox. 2014). Before these benefits have scientifically proven, though, I would like to remind you that exercise can induce similar increases in epinephrine, subsequent increases in IL10 and corresponding decreases of various inflammatory cytokines (Brandt. 2010, Petersen. 2005 & 2006; just as simply injecting or increasing epinephrine by other means will | Van Der Poll. 1997), albeit in response to exercise alone, not in response to endotoxin exposure. Whether the response to this stressor would be similarly conditioned and would thus affect endotoxin assaults, has imho not been investigated | Comment!

References:

• Brandt, Claus, and Bente K. Pedersen. "The role of exercise-induced myokines in muscle homeostasis and the defense against chronic diseases." BioMed Research International 2010 (2010).
• Kox, Matthijs, et al. "Voluntary activation of the sympathetic nervous system and attenuation of the innate immune response in humans." Proceedings of the National Academy of Sciences 111.20 (2014): 7379-7384.
• Pedersen, Bente Klarlund, and Laurie Hoffman-Goetz. "Exercise and the immune system: regulation, integration, and adaptation." Physiological reviews 80.3 (2000): 1055-1081.
• Petersen, Anne Marie W., and Bente Klarlund Pedersen. "The anti-inflammatory effect of exercise." Journal of applied physiology 98.4 (2005): 1154-1162.
• Petersen, A., and B. Pedersen. "The role of IL-6 in mediating the anti inflammatory." J Physiol Pharmacol 57 (2006): 43-51.
• Van Der Poll, Tom, and Stephen F. Lowry. "Epinephrine inhibits endotoxin-induced IL-1β production: roles of tumor necrosis factor-α and IL-10." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 273.6 (1997): R1885-R1890.

10 Days of 'Paleo Life in the Wilderness' Will Strip up to 18 cm off Your Waist and Boost Your Insulin Sensitivity by 53%

10 Days of 'Paleo Life in the Wilderness' Will Strip up to 18 cm off Your Waist and Boost Your Insulin Sensitivity by 53%

diet health insulin insulin sensitivity lifestyle lose fat metabolic syndrome paleo paleo lifestyle physical activity

Even though it may have been funny, this is not exactly how the scientists simulated the "paleo lifestyle" in the study at hand. Eventually, however, it came down to eating healthier, being active and even being stressed (within the limits of natural "paleo stress", though).

No, this science website is not going to turn into a paleo blog, ... don't worry. It's mere coincidence that this is the 2nd "paleo" study in 2 weeks that is interesting enough to get its own SuppVersity article devoted to it (last one).

Moreover, said study, which was published in the peer-reviewed scientific journal BioMed Research International, recently (Pruimboom. 2016), doesn't even have the world "paleo" in title of full-text and could still be called "the true paleo" study. It does, after all, revolve around a 10-day mimic of a "hunter-gatherer lifestyle" and its favorable effects on anthropometrics and clinical chemical indices such as the reductions in insulin, triglycerides, HDL, elevated liver health markers and other indices that are usually far from being optimal in the average student, scientist, physician, and other health professionals who participated in the study at hand.

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As the researchers point all, all subjects (n=10, n=32 and n=11) "were interested to experience the impact of ancient lifestyle on their own health and well-being and therefore jointly decided to engage in this study" (Pruimboom). In that, the term "this study" refers to three separate 10-day trips through the Spanish Pyrenees during the summers of 2011 (𝑛 = 10), 2012 (𝑛 = 32), and 2013 (𝑛 = 11), on which ...

"[t]he participants lived outdoors and walked from one watersource to another. Food was provided by the organization and with help of forest-guards from official institutes of the Catalan county. Food intake was planned before the trip, based on the average daily food intake by the traditionally living Hadzabe people in Tanzania. The use of mobile phones or other electronic devices was not allowed" (Pruimboom. 2016)

It is obviously debatable, if "mayonnaise" is a paleo food (not sure if they made it themselves) and how "paleo" the rest of the subjects' diet which may have been designed to mimic the macros, but probably not the foods of the Hadzabe (see Figure 1, tabular overview on the left) actually was.

Figure 1: Exemplary food intake (left) and changes in anthroprometrics (right); stat. sign. w/ p < 0.001 was observed for the median changes, not the minimal and maximal changes, obviously (Pruimboom. 2016).

What is undebatable, though, is the statistical significance and health relevance of the reductions in weight and body fat you can deduce from the sign. reduction in the median subjects' waist circumference.

Mind the statistics: There's a reason why I plotted more than one value in Figure 1. While I cannot tell you the reason why, I can tell you that at least one subject did not see the expected improvements in waist circumference. Possibly, he or she ate too much mayonnaise ;-), ... Why's that relevant? Well, it obviously goes to show you that calories still count. While the median subjects (with the low number of participants the scientists didn't calculate averages) obviously was in a caloric deficit, this one person probably just wasn't caught feasting secretly on the supply.

It should be noted, though, that these changes were certainly not attributable solely to the diet. Rather than that it should be obvious that the significant reduction in body and most certainly belly fat was the consequence of (a) what and how much the subjects ate while (b) experiencing what the Dutch scientists call "ancient stress factors" they were facing during a 10-day trip that revolved around the following four principles:

• Walking and limited manual work- providing the exercise / general physical activity stimulus modern humans lack: There were daily walking trips from waterhole to waterhole, with an average walking distance of about 14 km/day, including altitude differences up to approximately 1,000 m. The participants carried their own backpacks with an average weight of 8 kg. The trip took place in the part of the Pre-Pyrenees with a maximum altitude of 1,900 meters above sea level. In addition, some manual work was done to clean mountain trails as agreed upon with the Catalan Government.
• Intermittent fasting - leaving room to actually experience hunger and all its beneficial hormonal correlates (e.g. AMPK increase => mitochondrial housekeeping, etc.): Participants consumed two meals daily. The first meal was provided by the organization halfway and the second meal prepared on arrival at the camping site. Animals, including ducks, chickens, turkeys, rabbits, and fish, were delivered alive and killed by the participants. Fish were caught with nets in the Noguera river. All foods were prepared on the spot by the participants.
• 100% exposure to the elements - resynchronizing the internal clock: The participants slept outside in sleeping bags on small inflatable mattresses. Outside temperatures varied from 22 to 42∘C during daylight, whereas night temperatures varied from 12 to 21∘C. One group experienced a day of snow in the middle of July, which prompted the organization to provide hotel accommodations for a single night.
• Cyclic water intake - experiencing thirst to benefit from the anti-inflammatory release of oxytocin (Krause. 2011): Bulk (intermittent) drinking behavior was recommended by drinking as much as possible (up to satiety) after reaching a waterhole. The waterholes contained nonchloritized drinking water (Note: I would not suggest using "dehydration" as a means to improve your health; while it may have done this in the study at hand, it's simply stupid - and that's in the literal sense, as you've read in my article "Hydrated or Dumb").

Only in conjunction, with these "stress factors" did the diet do its body fat reducing and, as the data in Figure 2 shows, glucose and blood lipid reducing effects:

Figure 2: Changes in glucose and lipid metabolism over (I repeat) only 10 days; worth mentioning: all but the effect on HDL were statistically highly sign. with p < 0.001 (Pruimboom. 2016).

Effects of which the scientists say that they were the result of acute stress, which promotes release of stress hormones, including adrenaline, noradrenaline, and cortisol, all of which are bad in excess, but will "give rise to recovery from the reigning state of chronic low-grade inflammation and the return to homeostasis" (Pruimboom. 2016), when the stressors are hit the sweet spot of hormesis as it occurred in response to / corollary with the elevation in AST, ALT and hs-CRP of which I've explained previously that all of them can be natural reactions to (especially unaccustomed) physical activity (learn more about ALT, AST and exercise induced inflammation that may be misunderstood as a health problem).

In the study at hand, said "recovery from the reigning state of chronic low-grade inflammation" was characterized by "profound metabolic and immunologic adaptations", of which the scientists highlight that they relate to three classic features of the metabolic syndrome, i.e. body mass, glucose homeostasis, and circulating lipids. The fourth, i.e. blood pressure was - unfortunately - not recorded.

Ad-Libitum Paleo Diet W/ a Handful of Simple Rules Cuts 5-7 kg of Body Fat in 12 Weeks - Plus: Paleo Research Overview | more.

Bottom line: With the metabolic syndrome, also named the insulin resistance syndrome, being "a well-established risk factor for various diseases of affluence, including type 2 diabetes, cardiovascular disease, essential hypertension, polycystic ovary syndrome, nonalcoholic fattyliver disease, certain types of cancer (colon, breast, and pancreas), sleep apnea, and pregnancy complications, such as preeclampsia and gestational diabetes", the scientists are right to highlight in their conclusion that the subjects didn't just feel better subjectively (according to questionnaire), but returned from the "wilderness" in an objectively healthier state.

A state of which the scientists say that it has been promoted by the previously discussed consequences of the four pillars (see list) and related effects, such as the reduction of the postprandial inflammatory response (Holmer-Jensen. 2011; Klop. 2011; Peairs. 2011) and increased protection against pathogens (Fielding. 2000; MacEneaney. 2009) that occurs, when you are physically active before a meal. Even the presence of "cutaneous- and other body surface-directed danger signals" could, as Pruimboom et al. point out have been "hormetic triggers" | Comment!

References:

• Fielding, Roger A., et al. "Effects of prior exercise on eccentric exercise-induced neutrophilia and enzyme release." Medicine and science in sports and exercise 32.2 (2000): 359-364.
• Holmer-Jensen, Jens, et al. "Differential effects of dietary protein sources on postprandial low-grade inflammation after a single high fat meal in obese non-diabetic subjects." Nutrition journal 10.1 (2011): 1.
• Klop, Boudewijn, et al. "Understanding postprandial inflammation and its relationship to lifestyle behaviour and metabolic diseases." International journal of vascular medicine 2012 (2011).
• Krause, Eric G., et al. "Hydration state controls stress responsiveness and social behavior." The Journal of Neuroscience 31.14 (2011): 5470-5476.
• MacEneaney, Owen J., et al. "Effect of prior exercise on postprandial lipemia and markers of inflammation and endothelial activation in normal weight and overweight adolescent boys." European journal of applied physiology 106.5 (2009): 721-729.
• Peairs, Abigail D., Janet W. Rankin, and Yong Woo Lee. "Effects of acute ingestion of different fats on oxidative stress and inflammation in overweight and obese adults." Nutrition journal 10.1 (2011): 1.
• Pruimboom, Leo, et al. "Influence of a 10 days mimic of our ancient lifestyle on anthropometrics and parameters of metabolism and inflammation. The ‘Study of Origin’."

Ad-Libitum Paleo Diet W/ a Handful of Simple Rules Cuts 5-7 kg of Body Fat in 12 Weeks - Plus: Paleo Research Overview

Ad-Libitum Paleo Diet W/ a Handful of Simple Rules Cuts 5-7 kg of Body Fat in 12 Weeks - Plus: Paleo Research Overview

dieting health insulin resistance lean mass lose fat lose weight muscle loss paleo paleolithic eating whole foods

Yes, these foods were "allowed" - Even nuts, albeit in limited amounts.

Ok, I have to admit that I have repeatedly made fun of "paleo" in the past. Its "cultish", sometimes even "sectarian" appeal is and will remain as hilarious in my eyes as the (for some people life-or-death-)question whether certain foods "are paleo" or not (who cares, as long as they are healthy?). If you happen to have seen my presentation at the Paleo Convention in Berlin, last year, you will know that, despite my apathy against the quasi-religious sides of "paleo", I do appreciate a certain set of "rules" or "principles" (or whatever you may call them) all iterations of "paleo" have in common.

These principles work! And they have just been shown to help middle-aged type II diabetics (age 59±8 years) shed a quite impressive 6.7 kg of body fat (w/out exercise "only 5.7kg) in 12 weeks - without dieting as in not eating, although you're hungry (Otten. 2016).

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As the headline already tells you, the subjects, individuals diagnosed with type 2 diabetes within the past 10 years, who had a BMI of 25–40 kg/m2 and were weight stable (i.e. <5% weight loss) for 6 months (that's important, because otherwise the data on the energy deficit in Figure 1, which was calculated as baseline vs. study intake would be inaccurate) were allowed to eat "as-libitum", which practically means "as much as they wanted", as long, as they adhered to (a) "paleo foods", i.e. lean meat, fish, seafood, eggs, vegetables, fruits, berries, and nuts, but no cereals, dairy products, legumes, refined fats, refined sugars, and (extra) salt (canned fish and cold cuts like ham were allowed) and (b) followed the following simple food-specific rules:

• 

  Paleo Goes "Real Science" - First Meta-Analysis of Available RCTs Shows Improvements in Health + Body Composition | learn more

  eggs - maximally 1–2/day, and no more than 5/week,
• potatoes - only 1 medium sized potato per day
• dried fruit - 130 g/day, not more,
• nuts - 60 g/day, so no snacking on almonds 24/7
• rapeseed or olive oil - maximum 15 g/day
• honey and vinegar - only small amounts as flavoring in cooking
• coffee & tea - max 300 ml/day (each, I assume)
• red wine - only one glass per week

Since the participants were also instructed to drink mainly still water, you will probably not be surprised that all subjects, irrespective of whether they had been randomly assigned to the no exercise or exercise group ended up in a significant energy deficit - in spite of being allowed to eat "ad-libitum" (see Figure 1 for the most relevant information about their diet(s)).

Figure 1: Energy and macronutrient intake; differences, rel. + abs. above bars (Otten. 2016).

It is also not surprising that the extra-exercise (1h of exercise, 3x per week | details see blue box below) that was done on top of the (at least) 30 min of moderate intensity exercise like brisk walking all patients had been prescribed as part of their regular T2DM treatment, almost doubled the energy deficit of the subjects in the paleo + exercise, i.e. the PD-EX group (remember: the subjects were allowed to eat more, as long as they stuck to the previously presented rules - since the intake of foods like steak or chicken breast was not limited, they would have been able - within certain limits - to significantly increase their energy intake and still did not fully compensate the energy expended during the workouts; this should remind you of previous articles of mine outlining that "exercise does not just make you hungry" | learn more)

What about compli-ance? Both groups increased their relative intake of protein and their intake of monounsatu-rated and polyunsatu-rated fatty acids. Both groups lowered their intake of carbohydrates and saturated fatty acids. The reduction of sodium intake was only significant in the PD-EX group. Nine of the 14 participants in the PD-EX group completed the 36 exercise sessions according to the study protocol. The remaining five participants completed between 27 and 35 workouts during the study period. The participants in the PD-EX group increased the cumulative weight load (weight × repetitions × sets) with the leg press during one exercise session from 1350 kg (900−1800) to 3000 kg (2700−4000) after 12 weeks.

What did the 1h workouts look like? The PD-EX group underwent a program comprising a combination of aerobic exercise and resistance training in 1-h sessions three times weekly at the Sports Medicine unit at Umeå University. The exercise sessions were performed on weekdays, with at least 1 day of rest between sessions. They were supervised by experienced personal trainers with bachelor’s degrees in Sports Medicine.

All exercise sessions started with aerobic exercise. The first session of each week consisted of low-intensity aerobic training at 70% of the maximum heart rate on a crosstrainer (Monark Prime, XT 50, Vansbro, Sweden). The second session of the week consisted of ten high-intensity sprint intervals at 100% of the maximal workload on a cycle-ergometer (Monark, Ergomedic 839E, Vansbro, Sweden), with low-intensity cycling between the sprints. The third session of each week comprised six moderate-intensity 5-min intervals between 45 and 60% of maximal workload on a cycle-ergometer. The duration/workload of the intervals increased every other week. When necessary, the intensity of the aerobic exercise sessions was adjusted in accordance with the participant’s performance.

After the aerobic exercise, the sessions progressed to resistance training with both upper and lower body exercises, including leg presses, seated leg extensions, leg curls, hip raises, flat and incline bench presses, seated rows, dumbbell rows, lat pull-downs, shoulder raises, back extensions, burpees, sit-ups, step-ups, and wall ball shots. At each training session, the participant performed 3–5 of the aforementioned resistance exercises, with 10–15 repetitions and 2–4 sets. Once participants could complete all repetitions, the workload was increased for the following session.

Still, the main advantage of exercise was not, as you may now falsely expect due to the ~100% increase in energy deficit, a significantly increased loss of body fat (the latter did not double and that must not surprise you!). Neither was it a powerful increase in insulin sensitivity (HOMA-IR), which increased in both groups similarly (45% | p<0.001). Yeah, and even the extra 0.2% decrease in HbA1c, the sugar coating on the subjects' red blood cells  (-0.9% in diet only, -1.1% in diet + exercise), is not the main reason you must not miss your workouts while dieting (paleo-style or not ;-).

Figure 2: Fat mass (a), insulin sensitivity (b), and cardiovascular fitness (c and d) during 12 weeks following either a Paleolithic diet with a supervised exercise program (PD-EX) or a Paleolithic diet combined with general exercise recommendations (PD). Boxes represent medians and IQRs, whiskers represent the most extreme values besides outliers, and filled circles represent outliers (>1.5 IQR); **p<0 .01="" 2016="" p="" td="" tten.="">

So why are workouts important, then? It's the increased fitness, as evidenced by the PD-EX exclusive increase in maximum oxygen uptake (0.2 L/min) and the conservation of lean mass, which reached statistical significance (1.2kg in PD-EX vs. 2.6 kg in PD) only in the male subjects (p<0.05 for the difference between intervention groups), however (it is well possible that this is due to a lack of protein in the women's diet, cf. bottom line), that made / makes exercise (esp. resistance training) so valuable while dieting... this and another thing, the abstract of the study does not appreciate, because it did not reach statistical significance: The increase in relative resting energy expenditure (REE), the scientists observed in the PD-EX group (this adds to the extra energy expenditure during workouts, by the way!). While the relative REE didn't change in the PD group, it increased by a(n over the long-term) potentially relevant (but statistically non-significant) 3% in the PD-EX group - an effect that more than countered the nasty reduction in REE scientists still hold responsible for the yoyo-effect most "biggest losers" experience after successfully losing weight.

Is this the first paleo study? Even though, the number is still low, this is not the first one. In 2009, already, Jönssen et al. reported that "a 3-month study period, a paleolithic diet improved glycemic control and several cardiovascular risk factors compared to a diabetes diet in patients with type 2 diabetes" (Jönssen. 2009). In 2013, the same authors found that a "Paleolithic diet is more satiating per calorie than a diabetes diet in patients with type 2 dia-betes [and that t]he Paleolithic diet was seen as instrumental in weight loss, albeit it was difficult to adhere to" (Jönssen. 2013) - a result they had previously observed in patients with heart disease, too, when they compared a paleo to a Mediterranean diet (Jönssen. 2010), which also improve glucose tolerance less effectively than the paleo diet in said subject group (Lindeberg. 2007). Furthermore, studies in healthy individiuals Frassetto et al. (2015) like Österdahl et al. report that even "a short-term intervention showed some favourable effects by the diet" (Österdahl. 2008) such as weight loss, waist reductions and an improved quality of the diet and improved "BP [blood pressure] and glucose tolerance, decreases insulin secretion, increases insulin sensitivity and improves lipid profiles without weight loss" (Frassetto. 2015). In view of the fact that the less than a handful of long-term (>1 year), studies similar benefits when comparing paleo to other recommended diets, such as the Nordic Nutrition Recommendations in Mellbert et al. (2014) also show "greater beneficial effects" (e.g. fat mass, abdominal obesity and triglyceride levels just as they were observed by Ryberg, et al. in 2013) for the paleo diet(s), one could argue that the evidence in favor of paleo dieting in health and disease is slowly accumulating.

Eventually, diet is king, ... and that, just like the fact that doubling the energy deficit you have on paper won't double the loss of fat mass, shouldn't be news to you. That doesn't mean that dieting with exercise would not increase the loss of fat mass, but what is more important is that it helped the subjects - at least the male ones - maintain significantly more lean mass (=muscle and organ mass, which also affects you REE!).

Whether the failure of the workout to produce significant lean mass maintenance in the women was due to their sex, their hormonal status (the females included in the study were postmenopausal) or the fact that they gravitated to eat less protein (this is speculative, since the study does not provides sex-specific intakes) cannot be said. Even in the men, the lean mass loss is yet large enough to speculate that we'd have seen sign. less muscle loss with higher protein intakes. After all, the 79g the subjects in the PED-EX group consumed on a daily basis amount to only 0,84g protein per kg of body weight. This has repeatedly been shown to be too little for older individuals - even if they were not dieting. A follow up to the study which includes (a) simply more protein or (b) an extra protein shake after the workouts that would bump the subjects' total protein intake into the ~1.6-2.0g/kg region would thus be something I'd like to see in the (not so distant) future.

As long as said study will not have been done, though (something tells me that it won't ;-), you can still reference Otten's study as evidence that you can effectively lose weight without cereals, dairy products, and legumes... I have to admit, though, that I suspect that especially the latter two of these "forbidden" foods would rather have augmented, not messed with the improvements in body composition Otten et al. observed in the study at hand | Comment!

References:

• Frassetto, Lynda A., et al. "Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet." European journal of clinical nutrition 63.8 (2009): 947-955.
• Jönsson, Tommy, et al. "Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study." Cardiovasc Diabetol 8.35 (2009): 1-14.
• Jönsson, Tommy, et al. "A paleolithic diet is more satiating per calorie than a mediterranean-like diet in individuals with ischemic heart disease." Nutrition & metabolism 7.1 (2010): 1.
• Jönsson, Tommy, et al. "Subjective satiety and other experiences of a Paleolithic diet compared to a diabetes diet in patients with type 2 diabetes." Nutrition journal 12.1 (2013): 1.
• Mellberg, Caroline, et al. "Long-term effects of a palaeolithic-type diet in obese postmenopausal women: a two-year randomized trial." European journal of clinical nutrition 68.3 (2014): 350.
• Lindeberg, Staffan, et al. "A Palaeolithic diet improves glucose tolerance more than a Mediterranean-like diet in individuals with ischaemic heart disease." Diabetologia 50.9 (2007): 1795-1807.
• Österdahl, M., et al. "Effects of a short-term intervention with a paleolithic diet in healthy volunteers." European journal of clinical nutrition 62.5 (2008): 682-685.
• Otten, J, et al. "Effects of a Paleolithic diet with and without supervised exercise on fat mass, insulin sensitivity, and glycemic control: a randomized controlled trial in individuals with type 2 diabetes." Diabetes/Metabolism Research and Reviews (2016 |Accepted Article). doi: 10.1002/dmrr.2828
• Ryberg, Mats, et al. "A Palaeolithic‐type diet causes strong tissue‐specific effects on ectopic fat deposition in obese postmenopausal women." Journal of Internal medicine 274.1 (2013): 67-76.