Hydrogymnastics, Weight Training or Dance? What's the Best Workout to Achieve Your 2015 Physique Goals, Girls?

Do you really need a barbell or will hopping around in a group dance course or working out in the water aka hydrogymnastic suffice to build the 2015 cover model physique that's part of your new year's resolution? A recent Portuguese + Brazilian study may hold the answer to this "important" question.

It's about time to think about a good new year's resolution; and since any resolution that's aimed at losing weight and/or building a better physique, naturally involves exercise, the latest study from the University of Trás-os-Montes and Alto Douro comes right in time (Soares Costa de Mendonça. 2014).

The study that was conducted by Rosa Maria Soares Costa de Mendonça, Adenilson Targino de Araújo Júnior from the University of Trás-os-Montes and Alto Douro in Portugal, Maria do Socorro Cirilo de Sousa from the Federal Institute of Technology Education in Brazil and Helder Miguel Fernandes from the Research Centre for Sport in Portugal was designed to investigate the possible effects of 16 weeks of practicing different physical exercise programmes (strength training, dance or hydrogymnastics) on the body composition and anthropometric dimensions of adult women.

If you don't like any of the suggestions, try doing  HIIT instead!

Never Train To Burn Calories!

Tabata = 14.2kcal /min ≠ Fat Loss

30s Intervals + 2:1 Work/Rec.

Making HIIT a Hit Part I/II

Making HIIT a Hit Part II/II

HIIT Ain't For Everyone

The sample was comprised of 89 adult women aged 25–55 (41.42 ± 9.23 years), who were used to train at least three times a week and had no history of health issues that may compromise their ability to participate in the study. . Of these, 60% were married, 27% single and 12% divorced, all residing in the northeastern part of Brazil. As the scientists point out, ...

"[t]hese women were selected using a non probabilistic manner in specific locations, such as fitness clubs, hydrogymnastic gyms and a public municipal institution.

The sample was randomly divided into four groups, of which one was designed as the control group consisting of individuals that were sedentary (CG) (n = 25) and three were characterised as experimental groups:

• strength training (SG) (n = 25), in which the ladies trained three times per week under the supervision of a qualified trainer and did 3 sets of 8–12 repetitions (weights were progressively increased) with a 2–3 min rest period on each of the 50–60 workouts in which all the major muscle groups of the upper and lower limbs were exercised with the use of either machines with weights, free weights or resistance equipment,
• dance (DG) (n = 18), which the women trained three times per week at a moderate to vigorous intensity, which was defined as 60 to 85% of the maximum heart rate as identified by the calculation 220 – age for 50 to 60 minutes workouts involving activities activating all the major muscle groups in a continuous manner using basic steps and a minimum of three rhythmic variations of popular dance styles and aerobics per session with songs of a rhythmic cadence of 100 to 160 beats per minute, and
• hydrogymnastics (HG) (n = 21), in which the women trained with a frequency of three days per week at moderate to vigorous intensity, defined as 60 to 85% of the maximum heart rate using exercises that involved the major muscle groups of the upper and lower limbs with a focus on cardiorespiratory exercises, followed by muscular endurance exercises using equipment such as shin pads designed for hydrogymnastics, dumbbells, bars, plates, floating devices and pool edges with each exercise taking from 2 to 3 min to complete and the whole session lasting 45 to 55 min.

All workouts were designed according to the exercise routines from the ACSM guidelines (Garber. 2011) and the adherence to the exercise prescription was monitored by trained personnel. The workout duration and frequency were more or less identical and even the intensity was similar.

Figure 1: Changes in anthropometric parameters after 16 weeks of training (Soares Costa de Mendonça. 2014).

As you can see all training regimen lead to measurable improvements in the anthropometric parameters. Of the three different exercise regimen the "exotic", i.e. the hydrogymnastics training, was yet on overall the most effective "belly fat reducer" among the three training protocols.

Figure 2: Changes in body composition (calculated based on caliper data) after 16 weeks of hydrogymnastics, weight training, dance or idleness (Soares Costa de Mendonça. 2014).

Things look a bit different, when we take the body composition data the scientists calculated based on the skinfold measures into account: Here the strength training has a slight, but not necessarily significant edge over the hydrogymnastics (keep in mind that the efficacy of hydrogymnasticsmay partly be due to a novelty effect, i.e. new exercise = greater response | see fat mass loss after 8 vs. 16 weeks). Every ladies favorite, the group based dance exercise is yet - once again - trailing third.

Don't forget: Female Athletes' Body Composition Suffers From Chronic Energy Deficits | learn more

Bottom line: While it appears to be clear that (a) starting your next year as a couch potato is going to increase your waist line and body fat levels significantly (remember the ladies in the control group of the study at hand switched from training regularly to being sedentary for 16 weeks), it is not clear if lifting weights or doing hydrogymnastics, which involved some "weight training", as well is the better 2015 body recomposition exercise for women.

What appears to be clear, though, is that the highly popular dance courses are the least effective 2015 exercise protocol to follow, when your goal is to improve your body composition without dieting | Comment on Facebook!

References:

• Garber, Carol Ewing, et al. "American College of Sports Medicine position stand. Quantity and quality of exercise for developing and maintaining cardiorespiratory, musculoskeletal, and neuromotor fitness in apparently healthy adults: guidance for prescribing exercise." Medicine and science in sports and exercise 43.7 (2011): 1334-1359.
• Soares Costa de Mendonça, Rosa Maria, et al. "The Effects of Different Exercise Programmes on Female Body Composition." Journal of Human Kinetics 43.1 (2014): 67-78.

What's the Optimal Dose of Vitamin D3 for Lean, Normal-, Overweight & Obese Women With Established Vitamin D Deficiency to Get 25OHD Back into the Normal Range?

Both ladies are D-ficient, but will probably need profoundly different amounts of D3 to get their 25OHD back in range.

Actually, I guess, I don't really have to tell you that there is not going to be guest post by Adelfo Cerame, today. Adelfo is busy with the last weeks of school, but will be back as soon as he has passed all the tests. And while I am not sure, whether or not you would call the latest on vitamin D supplementation an adequate replacement for a contest prep update from "your's truly", I suppose that it's better than nothing to bridge the time that still remains until the SuppVersity  Science Round-Up on the Super Human Radio Network is going to air (the show starts at 12PM, EST; the Science-Round-Up airs in the 2nd hour and will thus begin at 1PM, EST; click here to listen live or wait for the podcast // update: now available).

I am honestly not yet sure what exactly we will cover today, but among the things I am still thinking about how we can squeeze them into a 1h show are...

• methylxanthines caffeine, theobromine and theophylline can bind to human DNA - what does that tell us about the purported health benefits of caffeine & co?
• caffeine prevents memory impairment - in this case in a model of sporadic Alzheimer's disease
• anti-Alzheimer's effect of CLA - plus a list of supplements that have been implicated in the prevention of Alzheimer's and other amyloid diseases such as Parkinson's, Cerebellar Ataxis, Amyotrophic lateral sclerosis and (hardly recognized as an amyloid disease) diabetes type II
• the effect of body weight on the benefits of circuit training in older women - turns out that those who need it the most, namely the obese, also see the greatest benefits
• Gum arabicum to ward off holiday weight gain - that this could actually work is at least what a recent human study would suggest
• more on vitamin E, resveratrol, soldiers don't get hurt in battle, but by geranium (DMAA), ...

I think there should be something for everyone of you. Plus: If everything works out, this is going to be the first show to air live via Skype, so no nagging land line echoes and noise any more.

Let's get to the D-news, now

The general consensus among the vitamin D advocates currently is that 2,000 IU of vitamin D3/day is the minimum you need to bring low levels of 25OHD back into the normal range. A soon-to-be-published study by Gallagher, Yalamanchili and Smith that's available ahead of print on the website of the Journal of Steroid Biochemistry and Molecular Biology does yet contradict this notion - at least for women with a body mass <25kg/m² even the meager RDA of 400IU would be enough (Gallagher. 2012). That said the concise paper actually describes the results of two, not just one experiment, with

• study 1 (ViDOS) being a one-year randomized, double-blind placebo controlled study (ViDOS – Vitamin D supplementation in Older Subjects) of increasing doses of vitamin D3 (400,  800, 1600, 2400, 3200, 4000 or 4800 IU/day vitamin D3 vs. placebo + calcium supplements to maintain calcium intake between 1,200-1,400mg/day) in 163 Caucasians, age 57–90 years; all vitamin D insufficienty, i.e. serum 25OHD ≤ 20 ng/ml (50 nmol/l), and 
• study 2 (STOP IT) being a 3-year intervention study of calcitriol 0.25 mcg (the active form of vitamin D) twice daily, conjugated estrogens 0.625 mg  daily, a combination of both and placebo in 488 elderly women, age 65–77 years

Body composition indices for the studies at hand (i.e. percentages of total and regional fat and fat-free mass) were measured by dual energy X-ray absorptiometry (DEXA Hologic Delphi) at baseline and after 12 months.

Figure 1: Mean total body weight, total body lean mass, total body fat mass and serum 25OHD in different BMI subgroups of study 2 (STOPIT); right, corresponding calculated ratios (based on Gallagher. 2012).

Even the baseline data in figure 1 does actually yield some insights into the relation of BMI, adiposity and 25OHD levels. While the data on the left already shows that the fat mass increases almost linearly across the BMI levels, while the lean mass remains relatively stable (with the highest value in the overweight group, though), the ratios I calculated and plotted on the right-hand side of figure 1 make it even more obvious clear: The lean / fat mass ratio scales with the BMI. With identical levels in the normal- and overweight individuals and significant increases and declines in the lightest and heaviest study participants. Moreover, the 25OHD vitamin D to fat mass ratio drops most significantly between the low BMI and the upper normal zone, where I suppose even most of the "healthy" individuals will be hovering around these days.

Being lean is a positive predictor of increases in 25OHD with supplementation

That this latent "chubbiness" of the average Westerner may be of particular significance in view of the negative / non-significant outcomes in many of the vitamin D supplementation trials, becomes self-evident, when you take a closer look at the data in figure 2, however you will have to realize that my plot which comprises above all the highly relevant relative changes (middle, marked in red) tells a different story than the original plot from the study showing only the absolute changes (left, but in form of a line graph).

Absolute, relative (compared to baseline) changes and total 25OHD levels (ng/ml) after supplementation with low, medium and high amounts of vitamin D3 in lean, normal, overweight and obese women (based on Gallagher. 2012)

Accordingly, the conclusion of the abstract, which says that "the response to vitamin D is dependent on body weight" and that "women with BMI <25 kg/m² develop much higher levels of serum 25OHD after vitamin D supplementation compared to those with BMI of >25 kg/m²" (Gallagher. 2012) may be correct, but is somewhat misleading as it is open to be interpreted as 'lean women respond most favorably to vitamin D supplementation' - an interpretation that is not really sustainable in view of the relative changes I calculated for figure 2  (middle), yet by no means as incredible as the abstract of another vitamin D study, I dessicated back in September (see "Stronger & Leaner or Fatter & Less Muscular W/ 4,000IU Vitamin D3 - What if Abstract and Data Tell Different Stories?")

Bottom line: The data from this most recent investigation into the differential response of lean, normal, overweight and obese women to vitamin D3 supplementation shows that the absolute increases appear on BMI and that...

• 

  Always take vitamin D with fatty foods! (see "A Fat D-Ficiency")

  low dose supplementation (400 or 800IU/day) is probably only sufficient to rise and maintain adequate vitamin D levels in lean women,
• medium dose supplementation (1,400 or 2,400IU/day) yields the most favorable outcomes in total 25OHD levels and 
• high dose supplementation (3,200, 4,000 or 4,800IU/day) does not yield additional benefits in either the the normal-, overweight and obese subgroup and only marginally higher levels in the lean women.

Overall the study at hand would thus support the notion that a daily vitamin D supplement containing ~2,000IU is the best way to get deficient levels back up, esp. for lean women it should be no problem to cut back to 2x the RDA, i.e. 800IU after normal vitamin D levels are achieved. For the rest, future studies will have to show if low dose supplementation is enough.

These longissimus dorsi slices of mice on a normal and a vitamin D3 supplemented diet show that supplemental vitamin D3 can be used as a fat synthesizer and meat tenderizer in "meat-producing animals". (learn more)

The often-heard hypothesis that the decreased response to vitamin D supplementation in the obese would be a result of the preferential storage of vitamin D in the adipose tissue was not supported by data of the Ghallagher study "there is no evidence from the dose response curves that in obesity serum 25OHD is being deposited in fat" (Gallagher. 2012). In view of the fact that contrary to total vitamin D, which is in fact preferentially stored in adipose tissue (78%) over lean muscle (14%), 25OHD stores are distributed much more evenly with 33% being stored in body fat and 20% in muscle tissue in omnivores like humans and swine (the data is in fact based on a study in pigs; cf. Jakobsen. 2007).

Lastly, a beneficial effect of increase / normalized vitamin D levels on lean or fat mass was (once again) not observed in any of the studies; and that despite the fact that "body fat was an independent predictor of serum PTH", which decreased in response to calcitriol supplementation in study 2 (which is actually more of an adjunct for correlative analysis and as a data source to compare the results of study 1 to). In other words, normalizing your vitamin D levels without taking appropriate measures to counter what's probably behind both, the nasty body fat and the low vitamin D level is not going to make you lean or musclar - at least as of now, it rather appears as if this was yet another instance, where we are - if anything - treating isolated symptoms instead of the root causes of the obesity epidemic.

References

• Gallagher JC, Yalamanchili V, Smith LM. The Effect Of Vitamin D Supplementation On Serum 25OHD In Thin And Obese Women. J Steroid Biochem Mol Biol. 2012 Dec 11.
• Jakobsen H, Maribo A, Bysted HM, Sommer OH. 25-Hydroxyvitamin D3 affects vitamin D status similar to vitamin D3 in pigs – but the meat produced has a lower content of vitamin D. British Journal of Nutrition. 2007; 98 908–913.
• Shephard RJ. Limits to the measurement of habitual physical activity by questionnaires. Br J Sports Med. 2003 Jun;37(3):197-206; discussion 206.

How to Switch Off Your Menstrual Cycle W/ Exercise & Dieting - More Than 22% Deficit ➯ Increased Risk of Menstrual Irregularities + Reduced (!) Weight Loss

Messing with your hormones won't help to reveal your abs, ladies!

I have written about this problem previously. Actually the whole SuppVersity "Athlete's Triad"-Series (read it) is remotely related to it: Women working out like hulk and eating like a sparrow. A behavior that leads to hormonal imbalances and amenorrhea very reliably.

So if you are wondering, why your menstrual cycle is messed up. Why you cannot get pregnant or why you simply stopped menstruating, ladies, this article is for you.

Needless to say that the same goes for male and female trainers, obviously, for whom the results of a very recent study from the Pennsylvania State University and the Penn State University College of Medicine (Williams. 2014).

Low T3 syndrome is also a result of dieting and a part of the (Female) Athletes Triad.

Female Athletes' Body Comp Suf- fers From Dieting

Female Athlete's Triad is not ex- clusively female

Female Athlete's Triad - A Vicious Cycle

Female Athlete's Triad - Recovery Part 1/3

Female Athlete's Triad - Recovery Part 2/3

Female Athlete's Triad - Recovery Part 3/3

The study Nancy I. Williams and her colleagues conducted was designed to confirm or refute the that there would be a dose-response relationship between the induction of menstrual disturbances (luteal phase defects, anovulation, and oligomenorrhea) and the magnitude of energy deficiency.

In other words, the researchers expected that higher energy deficits would incur a significantly greater incidence and more severe disturbances of their menstrual cycle disturbances. To evaluate their hypothesis, the researchers conducted a randomized prospective design that employed controlled feeding and supervised laboratory-based exercise over the course of three menstrual cycles in young, untrained, premenopausal, eumenorrheic women.

Table 1: Overview of the experimental procedures; MC=Menstrual Calendar | Note: Mid-study Body composition testing occurred during Intervention Cycle 2 for most subjects, but in some it occurred during Intervention Cycle 3 (Williams. 2014)

"The study was conducted over three years, with yearly cohorts recruited in the fall of the academic year and followed until the end of spring semester. The controlled feeding and exercise training began after the Screening and Baseline periods, each period lasting one menstrual cycle. All phases of the intervention were anchored to subjects’ menstrual cycles, and each study phase consisted of one menstrual cycle (Intervention Cycle 1, Intervention Cycle 2, Intervention Cycle 3). A post study period of one week where diet and exercise remained controlled allowed for post intervention measurements. The study design is illustrated in Table 1.

Group assignments were based on varying levels of energy deficiency created through a combination of caloric restriction and exercise such that one group remained in energy balance and four groups were in different degrees of an energy deficit. Repeated assessments of menstrual status, metabolic status, and body composition were conducted." (Williams. 2014)

The study was conducted with healthy young, weights-stable women, who had not evidence or history of disordered eating were aged 18 – 30 years, weighed 45 – 75kg and had a normal body fat level of 15 – 35%. The women didn't smoke, were not hormones or anti-contraceptives.

So what did the scientists do?

During the Baseline period, subjects were randomly assigned to an experimental group for the Intervention Cycles 1, 2, and 3 of the study. The goal of the subject groupings was to test the impact of varying levels of an energy deficit created by the combination of caloric restriction and exercise on menstrual function.

Most women ignore the risk of bone loss and only few know that the un- wanted "clinical sequelae", i.e. the nasty pathological consequences, of not eating enough and working out like a maniac include sign. increases in cardiovascular risk (O'Donnell. 2004)

The overlooked significance of hormonal imbalances: As Williams et al. point out, "[a] large body of evidence in a variety of mammalian species has demonstrated a causal link between chronic energy deficiency and the suppression of reproductive function involving the central inhibition of gonadotropin releasing hormone (GnRH) pulsatility" (Williams. 2014). In humans, long term energy deficiency can result in functional hypothalamic amenorrhea, (FHA) and therefore, decrease estrogen exposure, diminishing estrogen’s impact on bone, reproductive, and cardiovascular regulation, often resulting in bone loss (Rencken. 1996; Wade. 1996), stress fractures - specifically in athletes (Barrow. 1988; Bennel. 1999; Brukner. 1997), transient infertility, dyslipidemia, and impaired endothelial function (Friday. 1993, Hoch. 2007; O’Donnell. 2004).

Table 2: Baseline demographic characteristics of study subjects categorized by group (top) and energy balance parameters averaged across Intervention Cycles 1-3 for each group (bottom) - directly from Williams (2014)

They were assigned to either a control group that did not exercise and consumed an amount of calories estimated to maintain body weight, a control group that exercised, but received extra food calories to remain in energy balance (exercising controls or EXCON), or one of four groups that exercised and were prescribed reduced energy intake to create varying levels of an energy deficit (energy deficit or ED groups). ED groups were defined by an energy prescription comprised from the quantity of calories provided as food and the quantity of calories expended as exercise. ED groups were prescribed targeted reductions in energy intake (7 days/week) compared to their Baseline energy needs ranging from – 15% to – 30% in combination with prescribed increases in exercise energy expenditure (5 days/week) equivalent in calories to + 15% to + 30% of Baseline energy needs.

Starvation diets will also mess w/ your thyroid | learn more

So, how low can you go? The scientists fount that the estimates of the magnitude of energy deficiency associated with menstrual disturbances ranged from -22% (ED2) to -42% (ED3), reflecting an energy deficit of -470 to -810 kcal per day, respectively. In contrast to the what Williams et al. expected, the severity of menstrual disturbances, was not dependent on the magnitude of energy deficiency and is thus not a gauge to estimate how much more you'd have to eat to become fully functional again.

As the researchers point out, specifically, the initial four energy deficit groups were intended to represent 1) an increase of 15% kcals of exercise (15% deficit), 2) an increase of 30% kcals of exercise (30% deficit), 3) a decrease of 15% in dietary intake, combined with an increase of 15% of exercise, (30% deficit) and 4) a decrease of 30% in dietary intake, combined with an increase of 30% kcals of exercise (60% deficit).

Figure 1: Daily energy deficit (left) and corresponding menstrual irregularities (right) the Pennsylvanian researchers observed during the intervention (Williams. 2014)

As you can see in Figure 1 the plan worked out quite well and the original hypothesis that the severity of the energy deficit would correlate with the risk of overall risk of menstural irregularities. What is interesting, though, is that the overall linear increase was visible mostly for the luteal phase disturbances. Actual unovulatory cycles were observed only in groups ED2 & ED3, but - and this is important - for some women, it was enough to just work out to induce oligomenorrhic cycles, i.e. infrequent (or, in occasional usage, very light) menstruation.


Next to the menstrual irregularities, which were obviously what the scientists were actually interested in, the scientists also observed that the 34 subjects lost weight, 3.8 kg in the ED1 and - listen up ladies! - only 2.8 kg and 2.6 kg in the high(er) energy deficit groups ED2 and ED3 (no significant weight loss occurred in the exercise only, i.e. the EXCON group).

Figure 2: Amount of weight (in kg) the women in the four groups lost over the course of the complete study period (Williams. 2014)

Bottom line: Let me say this right away. It's not unfair, but very clever that nature made sure that starving women cannot become pregnant.

If you look at the "target outcome" of most women's dietary interventions, i.e. the amount of weight they lose (see Figure 2), you will also have to concede that what many women believe would be "unfair" actually protects them from ineffective starvation diets. It was after all not the group with the highest, but the group with the lowest energy deficit that lost the most weight. So, ladies, be sure to remember this and if you are still not convinced that starving yourself is not the magical weight loss solution that will give you the "shape cover model" body you're looking for, take another look at the "9 Rules of Sensible & Effective Dieting" | Comment on Facebook.

References:

• Barrow, Gray W., and Subrata Saha. "Menstrual irregularity and stress fractures in collegiate female distance runners." The American journal of sports medicine 16.3 (1988): 209-216.
• Bennell, Kim, et al. "Risk factors for stress fractures." Sports Medicine 28.2 (1999): 91-122.
• Brukner, Peter, and Kim Bennell. "Stress fractures in female athletes." Sports Medicine 24.6 (1997): 419-429.
• Friday, Karen E., et al. "Elevated plasma low-density lipoprotein and high-density lipoprotein cholesterol levels in amenorrheic athletes: effects of endogenous hormone status and nutrient intake." The Journal of Clinical Endocrinology & Metabolism 77.6 (1993): 1605-1609.
• Hoch, Anne Z., et al. "Athletic amenorrhea and endothelial dysfunction." Wisconsin Medical Journal 106.2 (2007).
• O’Donnell, Emma, and Mary Jane De Souza. "The Cardiovascular Effects of Chronic Hypoestrogenism in Amenorrhoeic Athletes." Sports Medicine 34.9 (2004): 601-627.
• Rencken, Monica L., Charles H. Chesnut, and Barbara L. Drinkwater. "Bone density at multiple skeletal sites in amenorrheic athletes." Jama 276.3 (1996): 238-240.
• Wade, GEORGE N., JILL E. Schneider, and H. Y. Li. "Control of fertility by metabolic cues." American Journal of Physiology-Endocrinology And Metabolism 270.1 (1996): E1-E19.
• Williams, Nancy I., et al. "Magnitude of daily energy deficit predicts frequency but not severity of menstrual disturbances associated with exercise and caloric restriction." American Journal of Physiology-Endocrinology and Metabolism (2014): ajpendo-00386.

"Milk Kills," Study Says and Everyone is Afraid. Is This More Than Fearmongering Bullsh*t? Methodological Issues & Conflicting Evidence Would Suggest the Answer is "No!"

After reading this article you won't have to be afraid of milk any longer.

The editor of the British Medical Journal (BMJ) will be rubbing his / her hands. The paper by Karl Michaëlsson et al. (2014) that was published earlier this week, made it to the mainstream news in the US and Europe and did - at least at first sight - reflect well on his or her magazine. "The British Medical Journal saves you from intoxicating yourself with milk!" - That's great, right?

Well, in today's SuppVersity article, I am going to take a closer look at how "great" it actually is that studies like this hit the mainstream media, while less exciting, because beneficial studies on milk are not being mentioned at all ... unless, of course, it's the morally superior and allegedly healthier soy milk we are talking about *sarcastic laughter*

You can learn more about dairy at the SuppVersity

Dairy Has Branched-Chain Fatty Acids!

Is There Sth. Like a Dairy Weight Loss Miracle?

There is Good A2 and Bad A1 Dairy, True or False?

Lactulose For Your Gut & Overall Health

Is There a "Fat Advantage" for Dairy Lovers

Dairy, Diabetes, Estrogen, IGF-1, Cancer & More

Before we get to a detailed analysis of the analysis, let's briefly remind ourselves of the type of data we are dealing with. Data from the Swedish Mammography Cohort (all female subjects) and Cohort of Swedish Men (all male subjects) that was complemented by data from food questionnaire that were send out back in the late nineteen eighties (women) and -nineties (men) along with the invitation to participate in the respective cohort studies.

Figure 1: Flow chart of the study sample (Michaëlsson. 2014).

As you can see in Figure 1 we are dealing with a hell lot of data. Data of which we still should not forget that it is based on data of which Thompson, et al. were able to show that it has an accuracy of 45-52%, specifically for dairy products (Thompson. 2002).

Now, in the study by Thompson the subjects were asked about what they ate in the last 30 days. The data in the study at hand, however, is based on what subjects said about how often they drank milk in the past 365 days! A fact that is not likely to make the data any more accurate.

Furthermore, I assume that all of you will have heard of people who change their dietary habits over time, right? Well, for Michaëlsson et al. this is obviously news. Otherwise they would not have relied exclusively data that was gathered, when the subjects were enlisted for the cohort study in the late 1980s / 1990s, when they were trying to identify the reason that 15,541 of the men and women died over the course of the 10-20 year follow-up.
Speaking of 20 years. That's the time that passed between being enlisted and speculating about their daily food intake when the 90 303 women aged 39-74 were enlisted in the Swedish Mammography Cohort and the 31st of December 2010, which was used as an end point for the analysis.

Figure 2: Mortality raters (raw data) according to milk intake in glasses / grams (Michaëlsson. 2014).

Malicious gossip would now probably have it that the additional 10 year gap, i.e. 10 more years to start eating completely differently, alone, could explain why we see a significant negative effect of drinking milk in the female, but not the male participants, for whom the interlude between the food frequency questionnaire and the end point of the study was ~50% smaller.

Figure 3: Adjusted predictions of urine 8-iso-PGF2α, a marker of oxidative stress, in 892 women (based on cross sectional data, mean age 70 years) and 700 men (Michaëlsson. 2014).

A similar criticism can be brought forward with respect to the allegedly "objective" measurements of 8-iso-PGF2α, a marker of oxidative stress, that was assessed in only 892 women (based on cross sectional data, mean age 70 years) and only 700 men, i.e. 1.4% of the female and 1.5% of the male participants, where the "trend" towards increased inflammation reached - once gain! - significance only in the female study participants (see Figure 3).

Homogenization may in fact be a problem. You find that's bogus? There is evidence that suggests that homogenization, not pasteurization is a serious problem | more.

What do commenters say? If you take a closer look at the hitherto published comments (retrieved on October 31, 2015) on the BMJ website, you will find commenters mentioning (1) the obvious association between having too little calcium <> fractures and the desire to increase ones calcium intake by drinking more milk (Kerr, J. Prof. of Epidemiology in Columbia), (2) the absence (or as Rom R. Hill from the Newcastle University says "significant omission") of a clear distinction between raw and pasteurized milk and low fat and full fat milk that makes the study, in Kerr's eyes, more or less meaningless, (3) last but not least, an unknown commenter mentions the issue of hormone, antibiotics and analgesic abuse in modern milk production and highlights that somatotropin (rBST) was still allowed in the EU, when the data from the study was collected. In view of the fact that rBST can affect hormonal and metabolic growth factors including human serum insulin-like growth factors (IGF), this could be another reason specifically for an increase in cancer related mortality (Allen. 2002; WHO. 2006).

Learn more about dairy from Liz in a previous SuppVersity article, i.e. "Dairy - The Good, Bad or Ugly?"

Moreover, the hazard ratios you read of in the news may have been adjusted, but the question remains, whether the adjustment could correctly make up for the fact that men and/or women who consumed more milk, ...

1. consumed significantly more energy on a daily basis (39% more in women, 24% more in men),
2. consumed significantly more saturated (36% more in women) and total fat, and
3. were significantly less likely to use bone building calcium supplements (15 % less in women).

Of these three factors (1) + (2) could explain the increased mortality and cancer risk in women and (3) could explain why women, but not men have a higher risk of hip, but not general bone fracture (hypothetically!).

My recommendation: Don't overrate the results of the study at hand. It has truckloads of methodological shortcomings, a tinge of the hysterical attention grabbing sensationalism and, most importantly, it stand in stark contrast to previous results which indicate that...

Figure 4: If you look at all the evidence, you will see that milk is more likely to protect than to kill you (Elwood. 2008; Bonthuis. 2010; Goldbohm. 2011)

• a high intake of milk is associated with a 16% reduced risk of cardiovascular disease and an 8% reduced risk of diabetes, two of the most important health issues that will have you pass away years, if not decades before your time (Elwood. 2008 | meta-analysis of 15 pertinent studies),
• Australians with a high fat milk intake of of 339g/day or more have a 69% reduced risk of dying from cardiovascular disease than their peers (Bonthuis. 2010),
• Dutch full-fat dairy connoisseurs have a 1% reduced all-cause mortality risk for each 10g of full fat dairy consumption per day (Goldbohm. 2011).

And in spite of the fact that several other studies find no beneficial effects of milk consumption of CVD or all-cause mortality (e.g. non-significant -23% in partly adjusted model in the Whitehall II study), it appears very unlikely that "milk kills". That this statement makes appalling headlines and will get a lot of clicks on the Internet, on the other hand, stands out of question | Read the whole paper for free @ the BMJ Website make up your mind and tell me on Facebook what you think.

References:

• Allen, Naomi E., et al. "The associations of diet with serum insulin-like growth factor I and its main binding proteins in 292 women meat-eaters, vegetarians, and vegans." Cancer Epidemiology Biomarkers & Prevention 11.11 (2002): 1441-1448.
• Bonthuis, M., et al. "Dairy consumption and patterns of mortality of Australian adults." European journal of clinical nutrition 64.6 (2010): 569-577.
• Elwood, Peter C., et al. "The survival advantage of milk and dairy consumption: an overview of evidence from cohort studies of vascular diseases, diabetes and cancer." Journal of the American College of Nutrition 27.6 (2008): 723S-734S.
• Goldbohm, R. Alexandra, et al. "Dairy consumption and 10-y total and cardiovascular mortality: a prospective cohort study in the Netherlands." The American journal of clinical nutrition (2011): ajcn-000430.
• Michaëlsson, Karl, et al. "Milk intake and risk of mortality and fractures in women and men: cohort studies." BMJ 349 (2014): g6015.
• Thompson, Frances E., et al. "Cognitive research enhances accuracy of food frequency questionnaire reports: results of an experimental validation study." Journal of the American Dietetic Association 102.2 (2002): 212-225.
• WHO Expert Committee on Food Additives. "Toxicological evaluation of certain veterinary drug residues in food/prepared by the sixty-sixth meeting of the Joint FAO/WHO Expert Committee on Food Additives (JEFCA)." (2006).

Cumin as a Weight Loss Aid: 26% Greater Reduction in Waist Circumference, 32% More Body Fat Lost, Increased Conservation of Lean Mass in 88 Dieting Women

Is a small bowl of yogurt with 1.5g cumin better than every weight loss drug? Probably not, but if we go by the results of the study at hand, it's a damn effective adjunct to an energy reduced diet.

The figures in the headline of today's SuppVersity article certainly are impressive. The total weight loss, the 88 overweight / obese women who had been randomly assigned into two groups who dieted for 3 months either with or without the help of 3 g/d cumin powder with yogurt at two meals (each time 1.5 g cumin + 150 ml low-fat yogurt | the control group received the same amount of yogurt, but without cumin) on the other hand sounds less exciting.

6.2kg in the cumin and 4.19kg in the control group - that does not sound much for "obese / overweight" women. Luckily Iranian "obese women" are comparably slender compared to their Western counterparts. With a starting weight of 79.43kg in the active and 76.7kg in the control arm of the study, those 6.2kg and 4.19kg were thus -7.14% and -5.54% of the women's total body weight.

The results of the study at hand are nice, but one thing is missing: Exercise!

Tri- or Multi-Set Training for Body Recomp.?

Alternating Squat & Blood Pressure - Productive?

Pre-Exhaustion Exhausts Your Growth Potential

Full ROM ➯ Full Gains - Form Counts!

Battle the Rope to Get Ripped & Strong

Hula Hooping to Spot Reduce in the Midsection

In contrast to the starting weight the waist circumference of the ladies who participated in the study showed a borderline significant difference, with a non-significant advantage on part of the women in the control group whose waists were on average 3.2cm more slender.

Figure 1: As the data shows, the cumin supplement helped with both fat loss and lean mass conservation (Zare. 2014)

In view of the fact that fat mass and fat free mass were almost identical, I would yet not argue that this was an unfair advantage for the cumin group - I mean, you should be aware that the "weightier" you are, the more and more readily you will usually drop body weight, when you start doing the right things.

"But I have heard nigella sativa causes abnormal heart growth!" That's fortunately incorrect. Studies by Yar et al. (2008) indicate that high doses of cumin aka "nigella sativa" will lead to physiological cardiac hypertophy, with a "selective enhancement of the inotropic reserve" that's similar to the one "provoked by exercise training" (Yar. 2008). It is thus not really surprising that Dehkordi et al. (2008) observed that cumin exerts anti-, not pro-hypertensive effectsin patients with mild hypertension. Moreover, Al-Asoom et al. have recently been able to show that kumin supplements in combination with exercise "might be introduced as a new therapeutic strategy for the treatment of heart failure with superior advantages to exercise training alone" (Al-Asoom. 2014)

Figure 2: Blood lipids & fasting blood glucose improved as well (Zare. 2014)

Apropos, the "right thing" for all women in the study at hand was a diet that delivered 500kcal less energy than the women would have needed according to the well-known Harris-Benedict equation (learn more).

Obviously, this deficit was large enough to trigger a weight loss of approx. 1lbs per week in the cumin group, and 0.6lbs per week in the control group - and that in the absence of any restrictions in carbohydrates, fats or an additional exercise component (the latter is something I would strongly recommend if you plan to lose body fat, though).

So how and why did this work? That's certainly a warranted question. As of now, most of you knew cumin probably as a spice and maybe as a digestive aid (Milan. 2008) - not as a fat burner, glucose sensitizer, lipid drug and, if you dig somewhat further in the archives of peer-reviewed scientific journals, even as a nootropic (Bin Sayeed. 2013), right?

Table 1: Cumin seed oil will deliver most of the cholesterol controlling agents in a concentrated form (Ramadan. 2007)

Well, if you take a look at the literature you will learn that Cumin contains more than 100 different chemicals, including essential fatty acids and volatile oils, which have been shown to induce significant decreases in glucose, cholesterol, triglyceride and LDL levels and a significant increase in serum HDL levelsin previous rodent studies (Mohiti. 2011). In that, the lipid reducing effects of cumin could be attributed to (a) its glycoside saponins which inhibit the absorption of dietary cholesterol and increase its fecal excretion by interfering with its enterohepatic circulation and (b) its phytosterol content which will displace cholesterol from intestinal micelles and will thus further reduce the amount of absorbable cholesterol (Hayes. 2002; Ramadan. 2002 & 2007; ). The mechanism by which cumin reduces the blood glucose levels, however, is still not fully understood.

As Zare et al. point out, "the majority of these studies have been done on animals and the published human studies have been conducted on patients suffering from diabetes or hypercholesterolemia," which makes the study at hand that was conducted with healthy (albeit overweight) female subjects all the more important.

References:

• Al-Asoom, L. I., et al. "Effect of Nigella sativa Supplementation to Exercise Training in a Novel Model of Physiological Cardiac Hypertrophy." Cardiovascular toxicology (2014): 1-8. 
• Bin Sayeed, Muhammad Shahdaat, et al. "The effect of< i> Nigella sativa</i> Linn. seed on memory, attention and cognition in healthy human volunteers." Journal of ethnopharmacology 148.3 (2013): 780-786.
• Dehkordi, Farshad Roghani, and Amir Farhad Kamkhah. "Antihypertensive effect of Nigella sativa seed extract in patients with mild hypertension." Fundamental & clinical pharmacology 22.4 (2008): 447-452.
• Hayes, K. C., et al. "Free phytosterols effectively reduce plasma and liver cholesterol in gerbils fed cholesterol." The Journal of nutrition 132.7 (2002): 1983-1988.
• Milan, K. S., et al. "Enhancement of digestive enzymatic activity by cumin (Cuminum cyminum L.) and role of spent cumin as a bionutrient." Food chemistry 110.3 (2008): 678-683. 
• Mohiti Ardakani, J., Z. Akbarian, And A. Nazarian. "Effects Of Cumin (Cuminum Cyminum L) Oil On Serum Glucose And Lipid Levels Of Rats." Journal Of Shahid Sadoughi University Of Medical Sciences And Health Services (2011). 
• Ramadan, Mohamed F., and Jörg‐Th Mörsel. "Characterization of phospholipid composition of black cumin (Nigella sativa L.) seed oil." Food/Nahrung 46.4 (2002): 240-244.
• Ramadan, Mohamed Fawzy. "Nutritional value, functional properties and nutraceutical applications of black cumin (Nigella sativa L.): an overview." International journal of food science & technology 42.10 (2007): 1208-1218. 
• Yar, T., et al. "Effects of Nigella sativa supplementation for one month on cardiac reserve in rats." Indian J Physiol Pharmacol 52.2 (2008): 141-8.
• Zare, Roghayeh, et al. "Effect of cumin powder on body composition and lipid profile in overweight and obese women." Complementary Therapies in Clinical Practice (2014).