ONLINE DRIVERS MEDIA

Remember: If anything fructose from beverages (including juices), yet not fructose from whole fruit is a problem. In fact eating whole fruits will decrease your blood lipids and high sensitivity C reactive protein (hs-CRP) inflammation markers.

Fructose is bad for you, right? Right. According to the latest study from the University of Newcastle, the consumption of only one drink containing containing 50 g of either fructose or glucose or sucrose dissolved in water will have detrimental effects on the #1 indicator of whole body inflammation, which is high sensitivity C-reactive protein (hs-CRP).

Much to the researchers surprise, though, the same amount of fructose had significant beneficial effects on the plasma lipid levels of the healthy male and female adults (n = 14) between the ages of 18-60 years who were recruited by advertisement and underwent study procedures at the Nutraceuticals Research Group Clinic rooms at the University of Newcastle in Australia.
Since the exclusion criteria were: diagnosed hyperlipidaemia, diabetes, gastrointestinal disorders, currently on fructose/sugar restricted diet, vegan diet or weight loss program, undergone any surgical procedure for obesity, pregnant or lactating mother, taking lipid-lowering or anti-inflammatory drugs and BMI >30kg/m², the results may well be different in "sicker" individuals, but for the guys and gals who drank the three 50g "sugar" solutions on three different occasions after an overnight fast, the "negative effects" of fructose were far from being conclusive.

Figure 1: Changes in hs-CRP, HDL and LDL in response to the ingestion of the test drinks (Jameel. 2014).

Even if you belong to the ever-increasing numbers of brainwashed fructose haters who believe that fructose and not a general overconsumption of energy was to blame for the obesity epidemic, you will have to admit that the data in Figure 1 leaves the significance of concomitant increases in hs-CRP and significant improvements in the HDL/LDL ratio, as the scientists phrase it, "to be delineated when considering health effects of feeding fructose-rich diets" (Jameel. 2014).
Well, yes, but (a) its only an acute response and (b) while increased levels of hs-CRP have been found to be associated with heart disease (Rifai. 2001; Danesh. 2004), the same can be said for a high LDL/HDL ratio (Fernandez. 2008).

Figure 2: CRP-dependent risk levels for cardiovascular disease according to the American Hear Association.

If we also take into consideration that the baseline hs-CRP level of the subjects was 1.5mg/L and thus low to mid-range for the average Westerner (depending on his or her ethnicity | Albert. 2004), an increase of 10% to a maximal value of 1.65mg/L would not bring them to critical heights of which the Farmingham study says that they start at 3mg/L for Westerners (Wilson. 2005). Thats not ana optimal level, but considering the fact that we are talking about "average Joes and Janes" who probably dont work out, eat whatever they like and give a damn about their sleep hygiene (all three factors have previously been linked to elevated hs-CRP levels) thats not astonishing and has absolutely nothing to do with the ingestion of 50g of fructose.

Furthermore, a comparison of the predictive value of different risk markers for cardiovascular disease by Folsom, et al. (2006) indicates that the hs-CRP values did not add to the prognostic value of the standard risk factors which are age, race, sex, systolic blood pressure, smoking status, diabetes and - you guessed it - total and high density lipoprotein cholesterol, which increased by almost 7% while the amount of LDL dropped by maximally 6%. Thus the LDL/HDL ratio decreased from 1.84 to 1.62. Thats a 12% decrease that would be health relevant if the subjects LDL/HDL ratio was not far away from the danger-zone (>5 | see Manninen. 1992), already. Similarly, the total cholesterol to HDL ratio dropped by -1.97 but wasnt in the danger zone before, either.
References:

• Danesh, John, et al. "C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease." New England Journal of Medicine 350.14 (2004): 1387-1397. 
• Fernandez, Maria Luz, and Densie Webb. "The LDL to HDL cholesterol ratio as a valuable tool to evaluate coronary heart disease risk." Journal of the American College of Nutrition 27.1 (2008): 1-5.
• Folsom, Aaron R., et al. "An assessment of incremental coronary risk prediction using C-reactive protein and other novel risk markers: the atherosclerosis risk in communities study." Archives of internal medicine 166.13 (2006): 1368-1373. 
• Hermsdorff, Helen Hermana M., et al. "Research Fruit and vegetable consumption and proinflammatory gene expression from peripheral blood mononuclear cells in young adults: a translational study." (2010).
• Jameel, Faizan, et al. "Acute effects of feeding fructose, glucose and sucrose on blood lipid levels and systemic inflammation." Lipids in Health and Disease 13.1 (2014): 195.
• Manninen, Vesa, et al. "Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study. Implications for treatment." Circulation 85.1 (1992): 37-45.
• Oliveira, A., F. Rodriguez-Artalejo, and C. Lopes. "The association of fruits, vegetables, antioxidant vitamins and fibre intake with high-sensitivity C-reactive protein: sex and body mass index interactions." European journal of clinical nutrition 63.11 (2009): 1345-1352. 
• Ravn-Haren, Gitte, et al. "Intake of whole apples or clear apple juice has contrasting effects on plasma lipids in healthy volunteers." European journal of nutrition 52.8 (2013): 1875-1889.
• Rifai, Nader, and Paul M. Ridker. "High-sensitivity C-reactive protein: a novel and promising marker of coronary heart disease." Clinical chemistry 47.3 (2001): 403-411.
• Wilson, Peter WF, et al. "C-reactive protein and risk of cardiovascular disease in men and women from the Framingham Heart Study." Archives of internal medicine 165.21 (2005): 2473-2478.

This article will teach you how to make sure youll see your great, great grand children.

This is one of the many things I have learned from my good friend Carl Lanore, whose radio show, Super Human Radio, I have been following for years before I became what Carl once called "semi-famous": We, that is humans in general and researchers in particular, tend to focus way too much on the sophisticated, the innovative and the revolutionary stuff, when oftentimes the answer to ostensibly open question is lying openly before our eyes. Athletics and bodybuilding, is one of these areas, where practitioners have been doing everything right for decades... and what was their reward? World-records and mind-boggling physiques, for example.

This is yet by no means the only example. The "paleo movement", as bizarre and disfigured as it may have become does still exemplify that the same can be said of "healthy eating", as well.
There have always been people who (instinctively?) knew how to do it - hell, even the hailed Mediterranean Diet is no invention of brainy scientists (certainly not of dumb dietitians). And when we are honest, we dont need websites like Longecity and tons of useless supplements to make the most of our genetic longevity potential: We all know what we should do, but unfortunately, many of us tend to forget that we dont do what it takes to join the ranks of those people about whom Marilynn Larkin wrote in ther 1999 paper "Centenarians point the way to healthy ageing" (Larkin. 1999).

Todays SuppVersity article is an homage to these people and the well-known but often overlooked research on what helps and hinders us from joining the ranks of people like Betsy Baker (supposedly 113, when she died in 1955), Marie-Louise Meilleur (supposedly 117, when she died in 1988) or Jiroemon Kimura (supposedly 116, when he died last year). I mean, they must have done many things right and only few things wrong, right? Based on the contemporary evidence, Ive compiled a list of rules. I guess, neither Betsy or Marie-Louise, nor Jiroemon will have followed all of them to the "T", but hey, this leaves room for you to decide whether youd rather indulge in one or another passion or stick to all of them to the "T" top Marie-Louises 117 or Jiroemons 116 years of age :-)

• Use the available medical care to your advantage: Within the health and fitness community, the things our regular doctors can do for us have gotten a surprisingly bad rep. It does however stand out of question that the availability and use of modern medicine is one of the cornerstones of the ever-increasing longevity in centennials and other healthy elderly. From basic treatments to complicated operations, all these things the availability of which we usually take for granted has helped us (and the living centenarians) to do what Thomas Perls calls "to ‘compress morbidity’ and live most of our lives in good health, with only a short period of ill health at the end." (Perls. 1999)

  Figure 1: Luckily, your place of birth is not the only determinant of life expectancy; map depicts life expectancy (in years) at birth (created by Panagiotis V. Lazaridis based on WHO & CIA data in 2008)

  At first this may contradict findings Engberg et al. present in a paper with data from a 29-year follow-up of hospitalizations among 40 000 Danes born in 1905, but in the end, it should be obvious that the low hospitalization rates, the Danish researchers observed in centenarians and almost centenarians were rather a consequence than a cause of their longevity and probably also due to timely non-stationary medical interventions, when one of them actually got sick (Engberg. 2009)
• Dont smoke, or quit smoking: I know this should be obvious, but I guess too many people still believe that they must belong to the lucky few Lewin and Crimmins, the authors of a recent paper with the intruiging title "Not All Smokers Die Young: A Model for Hidden Heterogeneity within the Human Population." (Lewin. 2014) are interested in. Contrary to these (allegedly) genetic outliers, the majority of us will suffer a significant reduction in life expectancy. Estimations of the number of years youll lose range from a handful of years to up to 25% (Rogers. 1991). For a US citizen the latter would equal almost 16 years! Years, of which Susan T. Stewart et al. (2009) say that the average 18-year-old may reclaim 3.76 life-years and, more importantly, 5.16 quality-adjusted years, in which he or she is not hospitalized and wasting away, if they managed to avoid the getting overweight / obese instead.

• In fact, the increase in BMI after smoking sessation "overwhelmed the positive effects of declines in smoking in multiple scenarios" Stewart et al. calculated and reduced the benefits for an 18-year old to 0.71 years or 0.91 (Stewart. 2009).
  
  But dont worry, other studies report much more beneficial effects. Taylor et al. (2002), for example, estimate that the life expectancy among smokers who quit at age 35 will exceeded that of continuing smokers by 6.9 to 8.5 years for men and 6.1 to 7.7 years for women. And in spite of the fact that early smokers will obviously realize greater gains in life expectancy, even those even those who quit much later in life gained some benefits: among smokers who quit at age 65 years, men gained 1.4 to 2.0 years of life, and women gained 2.7 to 3.7 years.
• Avoid drinking alcohol in amounts >0.5 glasses of wine per day: Notwithstanding the overcited epidemiological evidence which suggests that a moderate alcohol consumption will have beneficial effects on your life-expectancy, the margin between "just enough" and "already too much" is simply too narrow for me to suggest you drink more than the literal half glass of wine thats supposed to lower the all-cause mortality risk of women by ~20-25% (Streppel. 2009).
  
  

  Table 1: Relative Risk for Major Chronic Disease Categories, by Gender and Average Drinking Category (Rehm. 2002)

  A high(er) level of alcohol consumption, on the other hand, has been found to be associated with a higher risk of hypertension, alcoholic cardiomyopathy, cancer, cerebrovascular events and dementia (Kloner. 2007) - a fact that should remind you that (a) the evidence regarding the possible health benefits of alcohol is uncertain, and that (b) alcohol may not benefit everyone who drink. Theoretically, genetic polymorphisms that make alcohol the panacea for one, could turn an in innocent glass of wine into a deadly poison for someone else (Hashimoto. 2002).
  
  And just in case the ambiguity of data aint reason enough for you to let go of all alcoholic beverages on at least360 of 365 days of the year, the data in Table 1 may convince you.
  
  If you take a closer look at "Drinking Category I", where youll find all the women who consume 0–19.99 g pure alcohol and all the men who consume 0–39.99 g pure alcohol every day (a glass of wine has ~13g), you will see that alcohol increases the risk of liver cirrhosis by 26%, hypertensive diseases and other CVD by 40% and 50%, is associated with 34% and 23% higher risk of epilepsy for women and men, respectively and increases the risk of all cancers esp. those of the esophagus (+80%) significantly.
  
  I am not sure about you, but for me this alone would be enough to get my sleep, diet and exercise regimen in check instead of trying to use alcohol as a means to reduce my CVD risk.
• Attend to relationships and friends: Individuality has become on of the / the (choose for yourself) highest good(s) of Western civilization and few people are aware that we are paying a very high price for that. The influence of social relations on mortality is, after all, well documented. A meta-analysis of 148 studies (308,849 participants followed for an average of 7.5 years) confirms that the quality of our social networks significantly predicts mortality (Holt-Lunstad. 2010).

  Figure 2: Weighted avg. effect sizes across different measures of social relationships (Holt-Lunstad. 2010).

  People with social relationships defined as adequate are 50% more likely to survive than older adults with social relationships defined as poor or insufficient. The overall effect remains consistent across age (see Figure 2).
  
  It is yet still unclear whether specific types of relationships are more advantageous than others. Giles et al. (2005) showed that the beneficial association between social networks and survival among elderly people may be restricted to relationships with friends and confidants rather than with children and relatives. In a meta-analysis of 53 prospective observational studies on older adults, marriage or support from a partner was found be a significant independent predictor of survival; the overall reduction in mortality risk was 9–15%. However, this association was statistically significant in only half of the studies (Manzoli. 2007).

• As Rizzuto & Fratiglioni (2014) point out, one hypothesis suggests that strong social connec tions can buffer significant stress and protect against ne ative stress-related outcomes:
  

  "People might be protected from adopting stress-related lifestyle choices that are detrimental to health, such as smoking, excessive alcohol consumption and sleep loss." (Rizzuto. 2014)

  The main-effect hypothesis postulates that social support is beneficial regardless of the stress level a person is experiencing; in other words, social support can act protectively even before a stressor is experienced. For instance, persons with social support could be influenced to engage in protective be haviors such as exercise.
  
  Moreover, having a wide range of social ties also provides multiple sources of information that could result in more effective use of available health care and services (Cohen. 2004). No wonder, you have, after all, read only a couple of days ago that education is what protects "poor women from fattening effects of rising wealth" in the SuppVersity Facebook News (read more).
• Stay lean and be avtive, God damnit! There is this unfortunate and die-hard myth of something scientists refer to as the obesity paradox. A term that is misrepresented by overweight journalists and doctors and misunderstood by the ever-increasing number of obese average Joes, for whom the misleading connotations of terms such as "healthy obese" are downright life-threatening. 
  
  And this is not an exaggeration, by the way. If you look at the 30% increase in mortality risk Whitlock et al. (2009) calculated based on a meta-analysis of data from 57 prospective studies that included almost 900,000 adults for every 5-point increase in BMI the attribute "life-threatening" is by no means an exaggeration.

• Although the proportional increase was greater at younger ages (35–59 years), the corresponding increase in mortality for those in their 70s was nearly 30%, and for those in their 80s, it was still 15% - the notion that older people would benefit from being fat is thus simply hilarious.
  
  Whats not hilarious, though, is that a certain amount of healthy, well-distributed body fat thats complemented by a decent amount of life-extending muscle mass (20% reduction in all cause-mortality for men >55years w/ a decent amount of lean mass; see  SuppVersity Facebook News | learn more) and a corresponding BMI between 20-27 offers enough energy reserves to draw on, when youre sick and old. It is thus also not surprising that being slightly overweight (obesity starts with BMI >30) is not a risk factor for people aged ? 65 years (Heiat. 2001) and certainly better than being what scientists call "underweight", when its actually only "undermuscled" for the vast majority of elderly individuals who are affected.

• As a SuppVersity reader you know: The risk for both, being underweight and overweight can be reduced if not nullified by a high amount of daily physical activity (the 10,000 steps mantra) and working out regularly. Being moderately active, alone, for example, was found to be associated with a 3.6x higher chance of "successful [=healthy] aging" in a recent study from the University of Ibadan - for regular vigorous activity, the chance of aging healthily increased by 711% (Gureje. 2014)!

• Miscellaneous, but worth mentioning: This is where I will list everything that popped up on my radar while doing the research, but did not really appear to make a good standalone item in the list. Things like having sex, for example. At least twice a week, to make sure that you dont increase your risk of  fatal coronary heart disease by 180%, guys (Ebrahim. 2002). And ther results Smith et al. presented 5 years before are even more promising: According to their study, each increase of 100 orgasms per year is associated with a 46% reduction in all-cause mortality risk (Smith. 1997)!

It is obviously true that some of the things that determine healthy aging are (still) out of your reach. Most prominently, your sex! Scientists are yet struggling to explain the underlying reasons of the sex-specific "longevity bias", but contemporary research would suggest that...

"[...]female centenarians likely exploited a healthier life-style and more favorable environmental conditions, owing to gender-specific cultural and anthropological characteristics" (Franceschi. 2000) 

... and do thus depend to a lesser extend on having the right mtDNA haplogroups, Thyrosine Hydroxilase, and IL-6 genes than men.

Figure 5: Yes, genes matter, but there is more (Franceschi. 2003)

Apropos genes, the "typically male" aka sex–dependent genetic predisposition to produce high levels of IL?6 is about as detrimental to your goal of making it past the "100+ years finish line" healthily, as being born with the nasty "?4" variety of the apolipoprotein E gene and the corresponding lifelong problems with high blood lipids and an increased risk of cardiovascular disease, Alzheimers & co (Panza. 1999; Bonafè. 2001).

Other genes that have been highlighted as factors that contribute to exceptional longevity are certain variants of the FOXO3A gene (Flachsbart. 2009), ...
References: 

• Berrington de Gonzalez, Amy, et al. "Body-mass index and mortality among 1.46 million white adults." New England Journal of Medicine 363.23 (2010): 2211-2219.
• Bonafè, Massimiliano, et al. "A gender–dependent genetic predisposition to produce high levels of IL?6 is detrimental for longevity." European journal of immunology 31.8 (2001): 2357-2361. 
• Cohen, Sheldon. "Social relationships and health." American psychologist 59.8 (2004): 676.
• Ebrahim, S., et al. "Sexual intercourse and risk of ischaemic stroke and coronary heart disease: the Caerphilly study." Journal of epidemiology and community health 56.2 (2002): 99-102.
• Flachsbart, Friederike, et al. "Association of FOXO3A variation with human longevity confirmed in German centenarians." Proceedings of the National Academy of Sciences 106.8 (2009): 2700-2705.
• Franceschi, C., et al. "Do men and women follow different trajectories to reach extreme longevity?." Aging Clinical and Experimental Research 12.2 (2000): 77-84. 
• Franceschi, C., and M. Bonafe. "Centenarians as a model for healthy aging." Biochemical Society Transactions 31.2 (2003): 457-461. 
• Giles, Lynne C., et al. "Effect of social networks on 10 year survival in very old Australians: the Australian longitudinal study of aging." Journal of Epidemiology and Community Health 59.7 (2005): 574-579. 
• Gureje, Oye, et al. "Profile and Determinants of Successful Aging in the Ibadan Study of Ageing." Journal of the American Geriatrics Society (2014).
• Heiat, Asefeh, Viola Vaccarino, and Harlan M. Krumholz. "An evidence-based assessment of federal guidelines for overweight and obesity as they apply to elderly persons." Archives of internal medicine 161.9 (2001): 1194-1203.
• Holt-Lunstad, Julianne, Timothy B. Smith, and J. Bradley Layton. "Social relationships and mortality risk: a meta-analytic review." PLoS medicine 7.7 (2010): e1000316. 
• Kilpeläinen, Tuomas O., et al. "Physical activity attenuates the influence of FTO variants on obesity risk: a meta-analysis of 218,166 adults and 19,268 children." PLoS medicine 8.11 (2011): e1001116.
• Kloner, Robert A., and Shereif H. Rezkalla. "To drink or not to drink? That is the question." Circulation 116.11 (2007): 1306-1317.
• Larkin, Marilynn. "Centenarians point the way to healthy ageing." The Lancet 353.9158 (1999): 1074.
• Manzoli, Lamberto, et al. "Marital status and mortality in the elderly: a systematic review and meta-analysis." Social science & medicine 64.1 (2007): 77-94. 
• Oliveira, Aldair J., et al. "The influence of social relationships on obesity: sex differences in a longitudinal study." Obesity 21.8 (2013): 1540-1547.
• Panza, Francesco, et al. "Decreased frequency of apolipoprotein E ?4 allele from Northern to Southern Europe in Alzheimers disease patients and centenarians." Neuroscience letters 277.1 (1999): 53-56.
• Perls, Thomas T., Margery Hutter Silver, and John F. Lauerman. Living to 100: Lessons in living to your maximum potential at any age. 1st ed. New York: Basic Books, 1999.
• Rehm, Jürgen, et al. "Alcohol-related morbidity and mortality." Mouth 140.208 (2002): C00-C97. 
• Rizzuto, D., and L. Fratiglioni. "Lifestyle Factors Related to Mortality and Survival: A Mini-Review." Gerontology (2014).
• Rodriguez, Beatriz L., et al. "Fish Intake May Limit the Increase in Risk of Coronary Heart Disease Morbidity and Mortality Among Heavy Smokers The Honolulu Heart Program." Circulation 94.5 (1996): 952-956. 
• Rogers, Richard G., and Eve Powell-Griner. "Life expectancies of cigarette smokers and nonsmokers in the United States." Social science & medicine 32.10 (1991): 1151-1159.
• Sebastiani, Paola, et al. "Genetic signatures of exceptional longevity in humans." Science 10 (2010): 1126. 
• Smith, George Davey, Stephen Frankel, and John Yarnell. "Sex and death: are they related? Findings from the Caerphilly cohort study." Bmj 315.7123 (1997): 1641-1644.
• Stewart, Susan T., David M. Cutler, and Allison B. Rosen. "Forecasting the effects of obesity and smoking on US life expectancy." New England Journal of Medicine 361.23 (2009): 2252-2260.
• Streppel, Martinette T., et al. "Long-term wine consumption is related to cardiovascular mortality and life expectancy independently of moderate alcohol intake: the Zutphen Study." Journal of epidemiology and community health 63.7 (2009): 534-540.

The study at hand used plain ascorbic acid, no quack supplements with "advanced vitamin C".

While people tend to believe that vitamin C is good for anything, the evidence that it actually does anything good is relatively scarce. Against that background I am happy to tell you that a group of Greek researchers from the School of Physical Education and Sport Science, the European University Cyprus and theAristotle University of Thessaloniki have now finally confirmed what many of you probably thought was a long-established fact: "[L]ow vitamin C concentration is linked with decreased physical performance and increased oxidative stress and that vitamin C supplementation decreases oxidative stress and might increase exercise performance only in those with low initial concentration of vitamin C." (Paschalis. 2014)
When they came up with the study design, Paschalis et al. simply assumed that the mythical ergogenic effect of vitamin C actually existed. To test this hypothesis, they screened 100 males for vitamin C baseline values in blood, picked the 10 individuals with the lowest and the 10 with the highest vitamin C values from their baseline sample and assigned them to two groups.

Figure 1: Overview of the study design (Paschalis. 2014)

Using a placebo-controlled crossover design, the 20 selected subjects performed aerobic exercise to exhaustion (oxidant stimulus) before and after vitamin C supplementation for 30 days.

An overview of the study design is shown in Fig. 1. All measurements were performed between 08:00 and 11:00 h after overnight fasting. Initially, to examine whether rest ing blood vitamin C concentration affects aerobic perfor mance, VO2max was assessed (using incremental cycling test to volitional exhaustion) and was compared in both the low and the high vitamin C groups (Monark, Vansbro, Swe den). More specifially, the protocol started with a 50 W load at 50 rpm and increased by 10 W every 2 min until volitional fatigue. The test was terminated when three of the following four criteria VO2max were met: (1) volitional fatigue, (2) a lower than 2 mL/kg/min increase in VO2 despite an increase in workload, (3) a respiratory exchange ratio greater than or equal to 1.10, and (4) heart rate within 10 bpm of the predicted maximal heart rate (220–age). Res piratory gas variables were measured using a metabolic cart (Quark b2, Cosmed, Italy), which was calibrated before each test using standard gases of known concentration. The VO 2max assessment was used as a reference value to cal culate the workload at the relative intensity of each subject and ensured that all subjects would cycle at similar relative intensity during the following aerobic exercise sessions.

After the baseline testing had been done, the subjects within both the low and the high vitamin C groups received either placebo (3x333mg of lactose) or vitamin C supplementation (3x333mg of vitamin C), in a double-blind randomized crossover fashion (see Figure 1).

Figure 2: Changes in VO2max (left) and redox status (right) in subjects according to initial vitamin C status before and after vitamin C supplementation for 30 days (Paschalis. 2014).

As you can see in Figure 2 there were measurable differences in the response to the acute exhaustive exercise protocol (an oxidant stimulus), the subjects in both groups performed before and after vitamin C or placebo supplementation for 30 days. The data in Figure 2 does yet also show that the subjects who had been randomly assigned to the vitamin C supplement group had lower baseline VO2max levels. A fact that raises the question whether this is the result of a lower vitamin C intake or whether the vitamin C intake correlates with an unhealthier lifestyle that left the subjects unfit and with low vitamin C levels.
Unfortunately, this question is hard to answer based on the available research on vitamin C. While we have conflicting results with respect to its ability to impair the adaptational response to exercise (Close. 2014), there is very little evidence that it will actually have beneficial effects on any meaningful performance parameters. In fact, a study by Huck et al. that was published in the scientific journal Nutrition in 2013 is probably what comes closest to the results of the study at hand.

Figure 3: Effects of 500mg vitamin C per day on selected parameters in a 4 week chronic exercise + diet supplementation in obese men and women (Huck. 2013)

In said study Huck et al. observed that the provision of 500mg of vitamin C as an adjunct to exercise and diet in obese individuals lead to significant reductions in heart rate and the ratings of perceived exertion during exercise. The data in in Figure 3 does yet also tell you that there were no beneficial effects on VO2max, which best reflects the adaptational response to exercise.

This results of stands in contrast to the study at hand, but in line with previous results of studies in athletes, where only more or less irrelevant reductions of the acute inflammatory response to exercise were observed (Nieman. 2000; Peters. 2001; Tauler. 2002). A response of which you as a SuppVersity reader know that it is an essential part of the signalling cascade that triggers the adaptational response to. If we eventually get back to the Paschalis study, it would thus appear that athletes who are usually consuming more than enough vitamin C in their diets and are not at particular risk of developing low serum vitamin C levels would see similar results as the "high vitamin C" subjects in the Paschalis study, i.e. none - even worse, in view of the potential negative effects on the training induced adaptations that could not become visible in the study at hand, because there was no exercise protocol involved, it could even harm their progress.
References:

• Close, G. L., and M. J. Jackson. "Antioxidants and exercise: a tale of the complexities of relating signalling processes to physiological function?." The Journal of physiology 592.8 (2014): 1721-1722.
• Huck, Corey J., et al. "Vitamin C status and perception of effort during exercise in obese adults adhering to a calorie-reduced diet." Nutrition 29.1 (2013): 42-45.
• Nieman, David C., et al. "Influence of vitamin C supplementation on cytokine changes following an ultramarathon." Journal of Interferon & Cytokine Research 20.11 (2000): 1029-1035.
• Paschilis, V. et al. "Low vitamin C values are linked with decreased physical performance and increased oxidative stress: reversal by vitamin C supplementation." Eur J Nutr (2014). Ahead of print.
• Paulsen, Gøran, et al. "Vitamin C and E supplementation hampers cellular adaptation to endurance training in humans: a double?blind, randomised, controlled trial." The Journal of physiology 592.8 (2014): 1887-1901.
• Peters, E. M., et al. "Vitamin C supplementation attenuates the increases in circulating cortisol, adrenaline and anti-inflammatory polypeptides following ultramarathon running." International journal of sports medicine 22.7 (2001): 537-543.
• Picklo, Matthew. "Supplementation with vitamin E and vitamin C inversely alters mitochondrial copy number and mitochondrial protein in obese, exercising rats (1030.5)." The FASEB Journal 28.1 Supplement (2014): 1030-5. 
• Powers, Scott K., et al. "Dietary antioxidants and exercise." Journal of sports sciences 22.1 (2004): 81-94.
• Powers, Scott K., And Kurt J. Sollanek. "Endurance Exercise And Antioxidant Supplementation: Sense Or Nonsense?-Part." Sports Science 27.137 (2014): 1-4.
• Tauler, P., et al. "Diet supplementation with vitamin E, vitamin C and ?-carotene cocktail enhances basal neutrophil antioxidant enzymes in athletes." Pflügers Archiv 443.5-6 (2002): 791-797.

Happy New Year! In case this guy looks anywhere similar to how you feel after yesterdays party night, todays SuppVersity article is for you!

"Happy New Year", health, love, ... you know the whole litany, so lets get over it and straight to the things that are really important, today. The hangover cures. In the following I have compiled an extensive yet probably by no means complete list of scientifically proven hangover cures that may help better than aspirin and plenty of water (Harvard Health Letter. 2006), alone.

Apropos aspirin, its actually not too bad to start with 400-800mg of it, if you are having a hangover. It has after been shown to block the increased prostaglandin synthesis in response to alcohol ingestion and thus counter at least the inflammatory aspect of the hangover (George. 1979).
The latter cannot be said of another common pain killer: Acetaminophen, which failed to inhibit ethanol-induced subjective effects in human volunteers in a 1992 study by Pickworth et al. The same study by George et al. would yet also suggest that aspirin may also prolong the time it takes for the alcohol to leave your system completely... and this may not be your only problem, because the coingestion of aspirin and alcohol has been associated with an increased risk of gastrointestinal haemorrhage (Needham. 1971).

So what do you do if water and aspirin are not enough? Well, here are a couple of suggestions - in a more or less random order, since there are hardly any studies that compare the efficacy of one to another.

• Figure 1: Effects of 200mg tolfenamic acid on hangover symptoms in man (Kaivola. 1983).

  Tolfenamic acid - Tolfenamic acid is a very specific prostaglandin biosynthesis inhibitor that lead to significant reductions in hangover symptoms in a 1983 study by Kaivola, et al. (see Figure 1).
  
  The only problem is: The subjects consumed the 200mg of the anti-migraine drug tolfenamic acid before they started binge drinking. Whether the effects are similarly pronounced if you take it the day after remains to be elucidated.
• Gamma linoleic acid (GLA) - The omega-6 fatty acid from vegetable oils like rapeseed/canola oil and soy beans, walnuts, flax seed (linseed oil), perilla, chia, and hemp seed effectively reduced the hangover symptoms of human volunteers in a study the results of which have unfortunately never been officially published (Moesgaard; based on Pittler. 2005).
  
  In view of the fact that I have only 2nd hand access to the results I cannot tell you how much GLA you would need. Considering the effect that the supplement contained B officinalis aka Borage, which contains 26-36% GLA, if its not specifically enriched, I would yet assume that 100-300mg should do.

Figure 2: Symptoms and possible contributers of hangover (Swift. 1998).

• Yeast + B-Vitamins: Another trial tested the efficacy of 250 mg dried yeast, 0.5 mg thiamine nitrate, 0.5 mg pyridoxine hydrochloride, and 0.5 mg riboflavin in participants who consumed vodka (40% volume alcohol) amounting to a total of 100 g absolute alcohol (Laas. 1999). The difference in the change for the symptoms discomfort, restlessness, and impatience was statistically significant in favor of the yeast preparation and appear to suggest that the corresponding supplement aka "Morning Fit" works.
  
  Moreover, corresponding research from the Chungnam National University in Korea shows that a preparation of combined glutathione-enriched yeast and rice embryo/soybean extracts constitutes a  "a promising candidate for improvements of alcoholic hangover" (Lee. 2009), as well.
• Oh!K - A hangover cure with green ginger, turmeric, pepper, and green tea extract, along with salt, citric and ascorbic acid and fructose as the carrier worked pretty well in a recent study by Gopi et al. (2014).
• Sprite! Or rather a sprite-like herbal drink - In the media you may have read about Sprite, when in fact the two drinks researchers from the Sun Yat-Sen University in China tested and found to be effective in increasing the production of the enzyme that helps our bodies to get rid of alcohol were xue bi, a fizzy lemon and lime drink of which the researchers did not declare that it was indeed Sprite and hui yi su da shui, probably a type of soda water (Li. 2014).
• After Affect(R): Another commercially available anti-hangover cure "proved" to be effective in a non-randomized non-controlled trial from the Utrecht University (Vester. 2012).
  

  Table 1: Rationale for the ingredients included in After-Effect©. 1 - Total dose of 5 capsules. 2 - Only those symptoms that showed a significant improvement during alcohol hangover are listed. GLA: gamma-linolenic acid, EPA: eicosapentaenoic acid (EPA), and DHA: docosahexaenoic acid (Verster. 2012).

  If it were not for the reasonable ingredient profile (see Table 1), I probably wouldnt have listed it, but with GLA, magnesium, B-vitamins & co it does contain a bunch of ingredients that may actually help.
• Party Smart (carbonate mix) - Yet another commercial preparation that contains calcium carbonate (615 mg) and vegetable carbon (345 mg) and has - unfortunately - to be consumed while you are drinking.
  
  More specifically, the subjects in the 2004 study by Manu et al. consumed their first serving of two caplets with first drink and two more caplets every 2 to 3 hours (or 5 to 6 drinks).
  

  Figure 3: Mean hangover score and mean blood alcohol 10h after drinking (Manu. 2004).

  The data in Figure 3 does yet indicate that this alkalization regimen worked pretty well (I wonder if sodium bicarbonate would to the same ;-) is a pretty effective means to (a) keep the hangover in check and (b) help your body clear the alcohol from your bloodstream.
• Aging! Ok, I know this does not really help you today, but maybe on New Years Eve 2065! Tolstrup et al. found that hangover following engagement in binge drinking is much more common in the young than in the older age groups (Tolstrup. 2014). For women, similar results were obtained.
  
  As the scientists point out, "[t]his finding could not be explained by the usual amount of alcohol consumption, frequency of binge drinking, or the proportion of alcohol consumed with meals" (Tolstrup. 2014).

References:

• George, Frank R., and Allan C. Collins. "Prostaglandin synthetase inhibitors antagonize the depressant effects of ethanol." Pharmacology Biochemistry and Behavior 10.6 (1979): 865-869.
• Gopi, Sreeraj, et al. "Studies on the effectiveness, safety and tolerability of two doses of Anti Hangover Drink in Reducing Alcohol Induced Hangover Symptoms in Adult Male Social Drinkers." Int.J.Cur.Res.Aca.Rev. 2.8 (2014): 125-131.
• Harvard Health Letter. How to handle a hangover: drinking fluids may help with the morning-after misery from getting drunk. Harvard Health Letter 31.3(2006):3. 
• Kaivola, S., et al. "Hangover headache and prostaglandins: prophylactic treatment with tolfenamic acid." Cephalalgia 3.1 (1983): 31-36. 
• Laas I. A double-blind placebo-controlled study on the effects of Morning Fit on hangover symptoms after a high level of alcohol consumption in healthy volunteers. J Clin Res 1999;2: 9-15. 
• Lee, Heon-Sik, et al. "Effects of a preparation of combined glutathione-enriched yeast and rice embryo/soybean extracts on ethanol hangover." Journal of medicinal food 12.6 (2009): 1359-1367.
• Li, Sha, et al. "Effects of herbal infusions, tea and carbonated beverages on alcohol dehydrogenase and aldehyde dehydrogenase activity." Food & function 5.1 (2014): 42-49. 
• Manu, M. B., and S. A. Kolhapure. "Evaluation of the Efficacy and Safety of “PartySmart” in the Prevention of Alcohol-induced Hangover: A Prospective, Randomized, Double Blind, Comparative, Phase III Clinical Trial." INDIAN JOURNAL OF CLINICAL PRACTICE 15.7 (2004).
• Moesgaard S, Hansen NV. GLA effectively reduces hangovers. Pharma Nord Research, unpublished report. 
• Needham, C. D., et al. "Aspirin and alcohol in gastrointestinal haemorrhage." Gut 12.10 (1971): 819-821. 
• Pickworth, Wallace B., et al. "Acetaminophen fails to inhibit ethanol-induced subjective effects in human volunteers." Pharmacology Biochemistry and Behavior 41.1 (1992): 189-194.
• Pittler, Max H., et al. "Effectiveness of artichoke extract in preventing alcohol-induced hangovers: a randomized controlled trial." Canadian Medical Association Journal 169.12 (2003): 1269-1273.
• Pittler, Max H., Joris C. Verster, and Edzard Ernst. "Interventions for preventing or treating alcohol hangover: systematic review of randomised controlled trials." Bmj 331.7531 (2005): 1515-1518.
• Swift, Robert, and Dena Davidson. "Alcohol hangover." Alcohol Health Res World 22 (1998): 54-60. 
• Tolstrup, J. S., Stephens, R. and Grønbæk, M. (2014), Does the Severity of Hangovers Decline with Age? Survey of the Incidence of Hangover in Different Age Groups. Alcoholism: Clinical and Experimental Research, 38: 466–470. doi: 10.1111/acer.12238.
• Verster, J. C., and O. Berthélemy. "Consumer Satisfaction and Efficacy of the Hangover Cure After-Effect©." Advances in preventive medicine 2012 (2012).
• Wall, Tamara L., et al. "Hangover symptoms in Asian Americans with variations in the aldehyde dehydrogenase (ALDH2) gene." Journal of Studies on Alcohol and Drugs 61.1 (2000): 13.