Conventional vs. Organic: It's Not About Getting More, But Getting Less For Your Money. Less Pesticides, Dioxins & Co

Image 1: The Ökomonitoring program took a very different approach to the question whether or not organic products are worth the extra cost, they did not look for the additional edge, but rather the "subtractive edge", if you will, and tried to answer the question: "Can we even produce 'organically' in an increasingly polluted environment"; now ten years after the program started the answer appears to be "Yes!" (MLR. 2012a)

"Organic produce is no better than conventional! You are being ripped off!" Statements like this have made the headlines in the past couple of days and many people (obviously not you, though!) are scandalized or shaking their head haughtily uttering things "I knew it, and that's why I always buy the cheapest..." What both groups are missing, though is the simple fact that the question the scientists posed, or rather the question the journalists put to the forefront, i.e. "Are organically produced fruits and vegetables more nutritious?", is nonsensical, because it would imply that the absence of certain chemical agents and production methods would increase the amount of nutrients a plant puts into its fruit, leaves, roots or whatever. Since I have discussed this with my friend Carl Lanore on yesterday's joint SHR + SuppVersity News Round Up pretty extensively (in fact so extensive that we could not cover the other topics I had lined up - sorry for that, folks!), I won't go into more detail on that here, but simply repeat that the fallacy of this approach was part of my reasoning not to bore you with write-up / comment #5325 published that's been published on the bazillion of blogs within the past couple of days, but rather give you the long and short of a governmentally subsidized program that's been running for 10 years, now, here in Germany: the Ökomonitorin program of in Baden-Württemberg (this is one of the individual states here in Germany).

It's not about what's in there, but about what is not!

The researchers who are mainly working at the University of Stuttgart set out with a whole different research question than most of their colleagues. Rather than trying to answer loosely defined questions such as "What's better: Conventional or organic", they wanted to know whether or not it would even be possible to "produce organic" in an environment that is already profoundly polluted; and though I don't want to give away too much in advance, after 10 years and ten-thousands of samples of organic and conventional fruits, vegetables and animal products being analyzed the answer is "Yes it is!"

"Organic fruits and vegetables had on average 180x lower pesticide content than conventional products; and only 5% of the samples from organic produce were objectionable."

That's the conclusion the researchers in the 10-years special report that has been published in July 2012 (MLR. 2012b). Since I know that you don't content yourself with universalities like this (otherwise you would hardly be here ;-), I would like to invite you to let me walk you through some of the detailed results of the latest data from 2011, although this may not be the exact same goods you have (or haven't) been buying in the course of the last year (I just checked: Only ~6% of you are actually from Germany)

The good the bad and the equally ugly

While the general trend that emerges does in fact speak in favor of the organic products, a brief look at the data in figure 1 should suffice to see that despite the fact that the number of offenders, i.e. products with pesticide residues above the maximally allowed threshold is close to zero, even organic produce is far from being pesticide free.

Figure 1: Percentage of conventionally and organically produced products with detectable (those did not have to be above the allowed threshold levels!) pesticide residues (data based on MLR. 2012a)

Of all the categories I picked when I compiled figure 1 there are however four product categories that caught my eye immediately, because the "organic advantage" as you may call it, is particularly small, here: Wine, plant oils and processed fruit and vegetables (the latter category included frozen, usually relatively pesticide free, but also canned food and dried foods, as well as fruit jars etc.). Intriguingly, in all of those four the pesticides could (and in the case of the Wine, the researchers even proved that) have gotten into the food-chain during the processing / manufacturing process, as well - in other words processed and organic tend to be contrastive pairs.

Figure 2: Percentage of products with pesticide levels above the allowed threshold (data based on MLR. 2012a)

When it comes to the actual "offenders", i.e. those products with levels above what is officially allowed, here in Europe, there are actually seven of which I feel that they really stand out (one for each day of the week, isn't that great?):

Mothercorn, the "abortion fungus" of the middle ages, the first source of LSD and the result of inappropriately stored and subsequently moldy grains / flour being used in the production of breads, is a potential cause of auto-immune diseases and lethal toxicities.

The mothercorn (Claviceps purpurea) content [µg/kg] of multi-grain breads with rye and wholemeal rye bread (please mind the leap on the primary axis; data based on MLE. 2012a)

The ingestion of 2 mg of mothercorn does already lead to adverse reactions which range from nausea over headaches, and cramping to a loss of sensation in the extremities and vascular occlusions (the latter will also arise from chronic low-grade intoxications)- in pregnant women it will induce contractions of the uterus and spontaneous abortion. The ingestion of 5-10g of the ergot-alkaloids from the fungus kill an adult man... not exactly what you want to have in your bread, right? Not even in "harmless quantities" - which is what even the worst offenders would have to be considered, still.

• the processed foods - irrespective of whether you buy veggies or fruit, you can be sure that the contamination raises with every processing step; be smart not lazy and buy whole foods, learn how to prepare them and cook for yourself
• cereals - 3.4% of the "oh so healthy superfoods", of which at total 72% of the conventional and 36% of the organic ones contain pesticides, are also on the list of items even the European officials suggest you should better not eat, if you don't want to become sick
• legumes - another favorite of mainstream dietitians are not just among the worst offenders (24% of the conventionally produced legumes contain pesticides above the tolerable limit), they are also the only product where even the organic variety is not suitable for human consumption in 11% of the cases and as if that was not enough, the number of substances above that threshold amounts to 17 compounds in the conventional and 3 substances in the organically produced legumes
• leafy greens - the health food per se may not be among the worst offenders but in those 6.7% of the samples that had pesticides above the the threshold level, the scientist were able to identify 27(!) different pesticides (note: not all pesticides were found in all samples and the worst offenders were not broccoli & co, but rather salads)
• ginger (=ingwer)- the conventional variety something many people use to improve their health had higher than tolerable levels in 12.5% of the cases; a health food "gone unhealthy", if you will
• berries - they may not be among the worst offenders, but they are "versatile": With 5 different pesticides in the samples the scientists analyzed they can't compare with the processed veggies with 45 different pesticides, but are doing quite "well"
• exotic fruit and citrus fruit - while with them the conventional farmers obviously assume that the consumer would throw away the peel anyway; or, and this segues right into our next topic, there are no governmental controls and regulations in place; after all, you should be aware that Germany is not exactly the country to grow "exotic fruits" ;-)

If we seize on the notion of "it's not us, it's only the others that contaminate their produce, ship it to Europe (or the US) and poison us", we must however realize that things aren't so easy as they seem: While the German organic produce may in fact be the less polluted one, neither the Israelis nor the South Africans or Moroccans, but rather our European friends, the Italians are trying to poison us ;-)

Figure Y: "Worst offenders" statistics for the countries of origin of organic produce (based on MLR. 2012b)

Now, all jokes aside, it is simply not possible and probably also highly un-rewarding to replace one prejudice, i.e. all organic produce is good with another more sophisticated one such as all organic produce from Germany is good and everything from Italy, Egypt and Greece is poison. Therefore, it is probably also not so important that the intricacies of these statistics are meaningless for the majority of you who are (I just checked) US residents and not among the 6% "resident" (=German) SuppVersity students ;-)

Organic = Say no to GMO!?

With the different legislative situation here in Germany, the quantitative data on GMO "contamination" in figure 3 is probably likewise irrelevant for many of you, but with the production of GMO corn being banned, here in Germany, it does give you a sneak peak on what can happen if the government is willing to act on behalf of its people (the majority of Germans is against GMO) instead of the industry (in all fairness it must be said that it is the US and not the European, let alone the German agrar-industry that's constantly trying to push GMO corn and other produce into the German market).

Figure 4: Relative percantage of soy and soyproducts that has been genetically modified (MLR. 2012b)

Even among the conventional produce, the number of outliers was small - roughly 5% of conventional products contained <0.1% corn from genetically modified plants - a result which is probably also to be accounted for by the awareness of the industry that they will have to throw all their produce away once the GMO-skeptic consumers realize that product is contains significant amounts of genetically modified plants.

The data in figure 4 does yet also show that things look different for soy products, most of which are imported from countries where the production of GMO foods is actually allowed (like the US ;-) and even non-GMO crop can be exposed to cross-contamination. If we take a closer look and discard the annual variations, it does yet become obvious that the GMO content of organic products is just as their pesticide content still much lower than it is in conventional ones. What is pretty troublesome, though, is that in 2011 25% of the products that are advertised as "GMO free" contained small amounts (<0.1%) of genetically modified soy - for you, my American friends this means: Having a label alone does not protect you from "GMO fraud" ;-)

Eggs, salmon, animal productts and other notable observations and changes from 2002-2012

Before I'll conclude this post with a couple of notes on trends and general observations the scientists who have been working on the Ökomonitoring program over the past 10 years made and let you make up your own mind of "whether or not you feel that getting less is worth paying more", let me briefly address the issue of dioxin-laden organic eggs Carl and I have been talking about, yesterday, already:

Image 2: If you have not done so, already, I highly suggest you read my previous post "Urban Gardening: 12x More Cadmium in Your Tomatoes Than in the Conventional Produce? Plus: Domestic vs. Foreign - What's Healthier?". After all, your own organic tomatoes and other produce can be effected by the environment in which you grow them, as well.

• Not just organically produced eggs, but also organically produced salmon have on average higher levels of DDT, PCB and total dioxins (TEQ) and HCB, DDT2, PCB 153, Dieldrin, Endosulfan, Chlordan, Toxaphen, Tribromanisol, PBDE, respectively (note: wild salmon is almost free of any of the latter!)
• Those contaminations are not brought about by what the farmers do, but rather what they didn't do, i.e. make sure that their free ranging hens are not running around on toxic soils and their fish are not swimming in a toxic sea - and this is where the initial research question of the Ökomonitoring program, "Can we even produce organically?", must be answered with a somewhat shabby: "It depends" and the one parameter it depends on is the environment, to which the animals (and to a much lesser degree, the crop) are exposed
  

Now, the implications of this are not that all organic animal products are worse than their conventional counterparts (in fact the number of products without any residues is larger for the organic products, unfortunately those products which are contaminated contain much higher levels!), but rather that you have to be choosier and try not to rely on the label "organic", if you know your local farmer and trust him, you may be better off buying his non-organic eggs that those from an organic farm on contaminated land...

Find out if your area has contaminated soil by using the MyEnvironment search engine at epa.gov! Enter your area code and get the result right away. If you type in "Bronx New York", for example, you will learn that the major risk factor from air pollution is formaldehyde, that there are two final NPL sites and so on and so forth (thanks to Carl Lanore and Alisa Profumo for pointing this out on today's Casual Friday).

But enough of that let's wrap it up for today, with a couple of more or less unrelated, but interesting facts, the first of which is so important that I decided to repeat it, although I mentioned it at the beginning of the article, already:

What is Furan? Furan is a heterocyclic compound that has originally been used in the chemical manufacturing industry. It does however also occur during the combustion of coal and is a component of tobacco smoke, as well as in a number of heat processed food items such as canned and jarred foods and coffee (FDA. 2004). Furan is carcinogenic to rats and mice and was classified as ‘possibly carcinogenic to humans’ (International Agency for Research on Cancer, 1995; see as well Cordelli. 2010; Chen. 2012)

• on average 180x lower pesticide residues in organic fruits and veggies - that's the astonishing result after 10 years of Ökomonitoring
• no = ZERO pharamcologically active substances in any of the testes organic produces
• antibiotics residues in organic honey were reduced from 23% to 0% from 2003 to 2005; no complaints thereafter
• the mycotoxin load is about equally high in conventional and organic produce
• No significant differences in terms of organic contamination and pesticide residues exist between animal products; the dioxin load in eggs free ranging hens and organic salmon are exceptions to this rule (while levels spiked in 2009, when "buying organic" really took off over here and more and more farmers started producing "organic eggs", the levels have been slightly declining over the past years)
• the way organic coffee is roasted leads to increased furan levels in organically produced roast coffee
• the amount of acrylamide in cookies is equally high in organic vs. conventional products, the in organic chips is higher and the number of samples with levels above the 1,000µg/kg threshold is higher as well
• no differences were found in terms of trans fatty acids in ready-made meals
• organic softdrinks are free of preservatives
• no artificial colorings in organic sweets

Now it's up to you - organic, yes or no? And remember: We cannot always make everything 100% right, but that does not mean that you should give up trying.

References:

• Chen T, Williams TD, Mally A, Hamberger C, Mirbahai L, Hickling K, Chipman JK. Gene expression and epigenetic changes by furan in rat liver. Toxicology. 2012 Feb 26;292(2-3):63-70.
• Cordelli E, Leopardi P, Villani P, Marcon F, Macrì C, Caiola S, Siniscalchi E, Conti L, Eleuteri P, Malchiodi-Albedi F, Crebelli R. Toxic and genotoxic effects of oral administration of furan in mouse liver. Mutagenesis. 2010 May;25(3):305-14.
• Food and Drug Administration. Exploratory Data on Furan in Food, vol. 2011. 2004 < http://www.cfsan.fda.gov/∼dms/furandat.html >
• International Agency for Research on Cancer. Summaries & Evaluations, vol. 2011. 1995. 
• Ministerium für Ländlichen Raum, und Verbraucherschutz Baden-Württemberg (MLR). Ökomonitoring. Ökomonitoring Bericht für das Jahr 2011. June 2012b.
• Ministerium für Ländlichen Raum, und Verbraucherschutz Baden-Württemberg (MLR).Ökomonitoring. 10 Jahre Ökomonitoring. 2002 – 2011. Jubiläumssonderausgabe. June 2012b.

The Mango Formula: 1% Mango Pulp = Fenofibrate + Rosliglitazone. Freeze Dried Mango Pulp Improves Glucose Tolerance, Lipid Profile and Body Composition More Effectively Than Standard Medication.

Image 1: Mango pulp (image
from HAK Agro Foods)

You know it, I love it: Real food! Meat, fish, dairy, vegetables, and, yes, fruits! Consumed in reasonable amounts, the latter are by no means that problematic, as some "gurus" and "fear-mongers" out there on the Internet want you to believe (I wonder why!? Probably because they cannot stand the thought that others eat the delicious fruit, they forbid themselves?). The paper of Edralin A. Lucas and her colleagues which was published in the latest issue of the British Journal of Nutrition (Lucas. 2011), is only the latest in a series of papers which should remind you of the fact that whole fruits (not juices or highly processed stuff) are way more than potentially harmful fructose bombs.

For eight weeks, the scientists from the Oklahoma and Carolina State Universities put a group of male C57BL/J6 mice on one of six dietary regimen:

• normal rodent chow (AIN-93M) - 10% of the energy from fat
  
• high fat diet (based on Molnar. 2005 > "Diabetes induces endothelial dysfunction but does not increase neointimal formation in high-fat diet fed C57BL/6J mice" - 60% of the energy from fat
• high fat + 1% freeze dried mango pulp (FDM)
  
• high fat + 10% freeze dried mango pulp 
• high fat + fenofibrate (500mg/kg diet)
• high fat + rosiglitazone (50mg/kg diet)

Despite lower average food and energy intakes in the high fat vs. the normal chow group, the animals in the high fat group "had a higher percentage body fat and epididymal fat mass". The latter was accompanied by an overall lower percentage of fat free mass.

Figure 1: Effect of different dietary regimens on energy intake, body weight gain, body fat and fat free mass in mice after 8 weeks on the respective diets (data calculated based on Lucas. 2011)

In contrast to the final body weight after 8 weeks, which did not differ significantly between the treatment groups, both, the addition of freeze-dried mango pulp, as well as the medications, reduced the percentage of body fat and helped the high fat fed mice to maintain a healthy percentage of fat-free mass.

Figure 2: Cholesterol and glucose response in mice on different diets after 8 weeks
(data adopted from Lucas. 2011)

Surprisingly, supplementation with 1%, but not 10%, freeze dried mango pulp had similarly beneficial effects on blood glucose and HOMA-IR (measure of insulin resistance) as rosiglitazone. The changes in blood lipids (total, HDL and LDL cholesterol; triglycerides), on the other hand, "did not reach statistical significance" in either of the treatment groups.

Leptin and adiponectin levels of the mice, however, responded favorably to the freeze-dried mango diets:

Mice consuming the freeze-dried mango diets had significantly lower plasma leptin concentrations than those receiving the control and HF diets. Rosiglitazone and fenofibrate had effects on plasma leptin concentrations that were statistically similar to the control and the freeze-dried mango groups. Mice that received the HF + 1% freeze-dried mango diet had the highest plasma adiponectin concentrations [...]. The HF +10% freeze-dried mango diet had a similar effect on plasma adiponectin concentrations to that of control and HF + rosiglitazone diets.

The reduction of leptin levels and the concomitant increase in adiponectin levels even beyond those of the mice on the control diet the HF + 1% mango group experienced are tell-tale signs of increased leptin sensitivity and decreased adipose tissue inflammation, both hallmarks in the etiology of the metabolic syndrome.

So, if the beneficial effects on body composition (cf. figure 1) have not already convinced you, the latter should certainly make you think of (re-)incorporating the fleshy stone fruit belonging to the genus Mangifera from the tropics into your diet. With a dose equivalent of 1g/kg body weight in mice and 80mg/kg in humans, my standard model, an 80kg human being, would have to eat at least 1 3/4 mangos (550g mango, considering a 85% moisture content) a day to arrive at a similar load of bioactive compounds (per kg body weight), as the mice used in the study. In view of the higher efficacy of the 1% vs. the 10% enrichment and similar results in studies on blueberries (Prior. 2010), it may yet suffice to eat mango (or its freeze dried pulp) twice or thrice a week. And even if you eat just one mango per week, I bet this would still be healthier than fruitphobia ;-)

It's in the Peel - The Protective Hull of These 61 Super Fruits Can Ward Off Cancer: Prunes, Plums, Jujube, Kiwi, Pitaya, Apple, Banana, Lemon, Cherry, Kumquat, Pomelo,...

Peru Ground Cherries could be among the most potent fruity anti-cancer agents nature has to offer.

In all the hoopla around "anti-nutrients", people tend to forget that the majority of the hailed phenols, flavenoids etc. serve the very same purpose, they protect the fruit of certain plants. For a recent study from the School of Public Health and the Chinese Academy of Sciences in Guangzhou, as well as the Peking Univerity Fang Li et al. have now compiled an extensive list of fruits, their peels, pulp and seeds and the corresponding anti-proliferative activity, you may want to use as an anti-cancer shopping guide, when you are grocery shopping... and if you do so, don't peel them: the protective peel is where nature stores most of the stuff that kills cancer cells by having them suffocate in their own reactive oxygen species!

Keep in mind, while the fruits can kill cancer in the petri dish you would be asking too much if you expect to cure existing cancer by just eating one or to servings of the top items on the list below per day. In conjunction with the nutrition & exercise tips you receive on the SuppVersity every day, they may yet contribute their share to render you "cancer proof".

Table 1: Anti lung-, breast-, liver- and colon-cancer activity of 61 fruits,  or rather their pulp, their peel and their seeds; marked in green are all values that are larger than the mean + 60% of the standard devidation (Li. 2013)

I have been thinking for quite some time about the optimal way to present the data, to pick a TOP10 or to come up with a selection and then realized that I - if I were in your position - would like to take a look at the data myself.

Instead of telling you what I thought were the most remarkable results I did thus decide to simply confront you with the complete data marking every value that is at least 60% above the mean + one standard deviation in green and ordering the data by the mean protective effect against the three different cancer types (lung, breast, liver, colon cancer) the researchers have tested for.

If you just take a cursory look at the data, the most striking observation the scientists made is unquestionably, the overall potency of the fruit polyphenols. What you have to keep in mind though is that we are talking about in-vitro studies and direct exposure to dosages of 50.09–141.79 mg/mL, as they were necessary to actually kill breast cancer cells are probably something you will never achieve no matter how many Peru ground cherries you eat. With the latter being among the most potent fruity anti-cancer "meds" we have, it is obvious that the question we will still have to answer pertains to the effects of actually eating any of these items.

It appears out of question that it's not going to hurt you. It should also be obvious that eating a packed of cherries is not going to rid you of existing cancerous growth. On the other hand, there is already plenty of evidence that

• cherries (in this case tart cherries) administered in an extract form, can reduce the risk of colon cancer in rodent models (Kang. 2003)
• polyphenol-rich cloudy apples juices can protect against gastric diseases associated with cancer formation (Graziani. 2005)

etc. The picture that's emerging though is that the in-vivo effects of the above and other fruit polypenols are more or less locally, namely in the gut, where the individual cell is directly exposed to a high amount of the active ingredients in the respective fruit. To achieve maximal benefits and actually battle cancer in other parts of our body than the gut, it may thus be necessary to isolate the molecules, compound them and inject them locally in the the cancerous tissue...

---

Bottom line: While consuming high amounts of these anti-cancer fruits will have a plethora of health benefits, which will eventually protect you from cancer in all parts of your body, using them as a druglike medicine in our "war against cancer" would warrant extraction and isolation procedures that allow us to apply them in high concentrations to certain parts of our bodies.

I would bet money that all of the "superfruits" in the list above, also help to avoid prostate cancer

Suggested read & podcast: Last weeks' special issue of the SuppVersity Science Round-Up on prostate cancer is certainly something you either have remembered, when you went through the items on the list. And yes, while the scientists did not test for it, you bet that all of the "superfruits" in the list will also be good for your prostate. And just in case you missed the last installment of the Science RoundUp, I'd highly recommend you briefly go back to the corresponding seconds to read and listen to all the details | learn more about prostate cancer...

Although I doubt that isolating the nutrients and developing corresponding delivery systems entails insurmountable technical difficulties (in fact corresponding nano-technology would probably be available, already; cf. Khandelia. 2013), I am pretty sure nobody is going to do this; after all, the compounds themselves would not only be non-patentable, because naturally sourced, they would also compromise the sales of conventional cancer drugs and are thus a red rag to any of the big players in the business public health has become.

References:

• Graziani G, D'Argenio G, Tuccillo C, Loguercio C, Ritieni A, Morisco F, Del Vecchio Blanco C, Fogliano V, Romano M. Apple polyphenol extracts prevent damage to human gastric epithelial cells in vitro and to rat gastric mucosa in vivo. Gut. 2005 Feb;54(2):193-200.
• Kang SY, Seeram NP, Nair MG, Bourquin LD. Tart cherry anthocyanins inhibit tumor development in Apc(Min) mice and reduce proliferation of human colon cancer cells. Cancer Lett. 2003 May 8;194(1):13-9.
• Khandelia R, Jaiswal A, Ghosh SS, Chattopadhyay A. Gold Nanoparticle-Protein Agglomerates as Versatile Nanocarriers for Drug Delivery. Small. 2013 Feb 27. 
• Li F, Li S, Li HB, Deng GF, Ling WH, Wu S, Xu XR, Chen F. Antiproliferative activity of peels, pulps and seeds of 61 fruits. Journal of Functional Foods. 20 May 2013.

Glucose vs. Fructose and Their Effects on Glucose, Insulin & Fat Oxidation in Men on Both Ends of the BMI Spectrum

"Fructose handles"? "Glucose handles"? "Saturated fat handles"? No, just the net result of a trashy diet.

I don't have to tell you that I don't buy into the "fructose is the devil" hysteria that's rampant in the blogosphere and certain parts of the scientific community. It's a matter of quantity and quality that determines the toxicity of a poison and in most of the "convincing" evidence on the detrimental effects fructose. I mean let's be honest, you don't have to be a rocket scientists to figure out that 5+ cans of Coke a day cannot be good for you (cf. "Fat Content Per Energy Drink 0g, Body Fat Gain Per Energy Drink 18g!"; read more) "194 Bananas in Three Weeks", on the other hand, are nothing to be afraid of (learn why).Have we been fooled again or is it just a high fructose corn syrup producer conspiracy?

Enough of the rants, let's get to the facts!

I guess that's enough for the "ranty" introduction. Let's now have a look at what a group of researchers from the School of Medicine in Portland has in stock for us: It's a paper titled "Change in postprandial substrate oxidation after a highfructose meal is related to body mass index in healthy men" that's about to be published in one of the future installments of Nutrition Research. As you will by now probably have figured out, the Anne C. Smeraglio and her colleagues had two things in mind, when they came up with the protocol that involved

• What did the subjects eat? Participants were fed an egg omelet, bagel with cream cheese, and sweetened beverage breakfast consisting of one-third of their estimated daily caloric. The meal consisted of 30% fat, 15% protein, and 55% CHO (as % of energy). The CHO energy was further divided into complex and simple CHOs; 25% of the total calories were from complex CHOs and 30% of the calories were from either glucose or fructose added to the beverage.
  12 healthy men without diabetes, with a mean age of 25 (23-31) years and a BMI less than 30 kg/m²,
• 2 visits at their labs that were separated by at least 1 week, but less than 1 month,
• two meals that were high in glucose or fructose which were served in random order as a breakfast after an overnight fast, and
• fasting for 7h after the ingestion of the standardized breakfast (sitting around watching TV or performing other, non-exciting quiet activities without the propensity to produce a catecholamine response)

During the experiment, the oxygen consumption and CO2 production were measured by indirect calorimetry to calculate resting energy expenditure and respiratory quotient (RQ; high RQ = burning predominantly glucose, low burning predominantly fat). The scientists also took blood samples at pre-defined intervals and collected the urine of their participants.

Figure 1: Insulin and glucose levels, as well as non protein respiratory quotient (high = carb oxidation; low = fat oxidation) 0-7h after the fructose and glucose breakfasts (Smeraglio. 2013)

The data in figure 1 is a summary of the the most "significant" results. In that the "quotation marks" enclosing the word "significant" is in my humble opinion the most significant information here - one that's encoded with irony, because after all, the only statistically significant effect the scientists observed were the ~2.5x higher insulin levels in the glucose group 60min after the ingestion of the test meal... yep, that's in the glucose group.

"There must be a mistake here!? Fructose is bad for you!"

The scientists have really done their homework as they did even take into account whether or not the amount of protein in the meals would have been responsible for differences in the respiratory quotient. The latter was not the case, the "baseline RQs between the fructose and glucose study visits were equivalent (0.82 ± 0.08 and 0.81 ± 0.10, respectively) and the p-value, indicating that there was a difference even rose from 0.72 to 0.75, when "when protein use was accounted for by evaluating NPRQ [non-protein respiratory quotient]" (Smeraglio. 2013)

Surprised? Well, I guess over all the lustig (=German for "funny") and unwarranted hoopla about how bad even small amounts of fructose are, you must have forgotten why scientists believed not too long ago that fructose could be the solution to, not the cause of the diabesity epidemic. After all, the paradigm of the mid to late 20th century was: Fructose does not spike glucose, so it should be the ideal sweetener for diabetics, because it is not necessary that your pancreas produces insulin to get rid of it.

I will not have to tell you, though that this assumption and the corresponding notion that totally replacing glucose with fructose would be a great idea is about as unwarranted, as the current fear of the "toxicity" of the small amounts fructose contained you'll be exposed to from a couple of pieces of fruit. I mean, let's take a peek at the data again.

Compared to the same amount of glucose, the consumption of the fructose equivalent of 5-6 medium sized (185g) apples (50-70g fructose, which is the amount of fructose the subjects in the study consumed) produces lower insulin levels and does not change either the leptin, triglyceride or glucose concentration in the blood or the ratio of glucose to fatty acid oxidation in healthy non-obese volunteers...

...apropos, non-obese, there was another thing to the headline wasn't there?

You are absolutely right, the research question involved (a) finding out what happens if you ingest a realistic breakfast where the carbohydrate content comes from (i) glucose or (ii) fructose and (b) determining whether the reaction would depend on the body weight / height² (BMI) ratio of the participants. So what about that, then? Let's see...

Did you know that there is a catalytic dose of ~40g of fructose per day (=6 normal size bananas) that will improve your glucose metabolism? (learn more)

"Although the absolute values for fat and CHO oxidation were not different between the fructose and glucose study visits, we did find a correlation between BMI and change in fat oxidation as a result of consuming the high-fructose meal compared with the high-glucose meal. The difference in fat oxidation (fat oxidation after the fructose meal minus fat oxidation after the glucose meal) was negatively correlated with BMI at the 4- and 7-hour time-points (Fig. 3; r =−0.59 [P= .04] andr=−0.59 [P= .04] for 4- and 7-hour time points, respectively) but not the 1-hour time point (Fig. 3; r=−0.52, P< .09). Nonprotein RQ displayed these same trends but did not reach significance." (Smeraglio. 2013)

As the scientists rightly point out, this suggests that the postprandial fat oxidation after the fructose meal was less than the fat oxidation after the glucose meal only among subjects with a higher BMI, and that the correlation with body weight, but not the difference itself was statistical significant.

Figure 2: Correlation of BMI with change in fat oxidation pearson correlation with linear regression trend lines between BMI and change in fat oxidation (fat oxidation after the fructose study visit minus fat oxidation after the glucose study visit; Smeraglio. 2013)

What's more, if you take a peek at the linear regression in the graph on the right hand side (figure 2) you will realize that that this does also mean that the fatty acid oxidation in lean individuals is actually increased after the ingestion of fructose. If I intended to drive my message "fructose from real foods is not your problem, folks!" home at all costs (which is what the "fructose is the devil" advocates like to do), I could seize on this observation and tell you: "Look folks, as long as you are already lean fructose will help, not impair your effort to get ridiculously shredded." I would yet hope that you are clever enough to see through this tactics and realize that neither the effect on the left hand side (=more fatty acid oxidation in the leaner folks with fructose vs. glucose), nor the one on the right hand side of figure 2 is physiologically relevant.

And that's not just because it's simply too small, but also because the ratio of glucose to fatty acid oxidation, i.e. the respiratory quotient (RQ) is not determining whether you store or lose body fat - if it were, you'd better be training in the "fat burning zone" for the rest of your (in that case) miserable lives.

---

Figure 3: Adding 7.5g of fructose ( to a 75g glucose load will improve not detoriate the glucose metabolism and that without increasing the amount of insulin that's released in response to the glucose load (Moore. 2000)

Bottom line: I am confident that that even without resorting to extreme interpretations of cherry picked data, the main message of today's article is clear. The comparatively small amounts of fructose you'll get right with the appropriate polyphenols & other cofactors from fruit and other fructose containing whole foods in your diet is not your enemy (Other items? Yeah, you know that even onions have 2g fructose, right?).

On a related note, you are aware that small amounts of fructose, like the 7.5g of fructose scientists added to the 75 g of glucose their 11 healthy subjects ingested during an oral glucose tolerance test had an up to 31% lower glucose response (these were the values for the 6 subjects with the highest level on the regular test) in the absence of concomitant increases in insulin response (see figure 3; Moore. 2000)!? You did not know that? Well, I guess it was about time to take a mental note, then ;-)

References:

• Moore MC, Cherrington AD, Mann SL, Davis SN. Acute fructose administration decreases the glycemic response to an oral glucose tolerance test in normal adults. J Clin Endocrinol Metab. 2000 Dec;85(12):4515-9. 
• Smeraglio AC, et al. Change in postprandial substrate oxidation after a high-fructose meal is related to body mass index in healthy men. Nutr Res.2013 [epub ahead of print]

Set to Be Obese? Epigenetic Programing in Utero - The Roles of Over- & Undernutrition, High & Low Protein, Fruits, Veggies, Zinc, Magnesium, Chromium, Vitamins & More

Image 1: Your mother's diet is not the sole cause of your love handles and health problems, but it could well have tipped the scale to your fat disadvantage. Don't be resentful, but don't repeat the same mistakes, either!

While it is certainly false to assume that anyone can't help but to get obese, it's similarly hard to deny that some people just have to cut back on the coke and sweets they eat to get back in shape, while others struggle with shedding superfluous weight (=fat) and regaining their health even if they are in a reasonable caloric deficit, eat a whole foods diet and exercise regularly. "It must be in my genes!" is what you will usually hear from people on both ends of the spectrum and while the former will smile at you and grab the next best snickers bar, just "to make sure that they don't lose too much weight", the unfortunate people on the other end of the spectrum are clutching to each and every straw, or, in these days of Internet quackery, "expert" advice to finally solve their life-long misery.

In today's blogpost I want to take a brief look at the leatest research into the epigenetic realities of obesity and how those nasty love-handles you have been carrying around for years, now, may actually have been "programmed" when what is now your body was still a bunch of constantly differentiating cells.

A fetus needs more than just adequate folate (let alone folic acid)

We have known for decades, that the consequences of fetal malnurishment, i.e. the insufficient provision of macro- and micronutrients, go well beyond an increase in infant morbidity and mortality. Van Assche et al. report as early as in 1977 that fetal growth retardation (due to malnurishment or other causes) was associated with reductions in both the size and the function of the pancreas (Assche. 1977); reductions, of which Hales et al. were able to show that they can lead to glucose intolerance and hypertension later in life (Hales. 1991).

Image 2: No, no, no! Juicing your fruits and downing 5-6 apples, oranges, peaches, lemons, grapefruits or whatever in one sitting is not healthy! Neither for you, nor for your offspring!

What can you do? As I said data from human studies is scarce and mostly observational, but if you are concerned about the beta-cell autoimmunity and subsequent increases in diabetes risk of your offspring, a study from the University of Tampare suggests that it may be a good idea to eat more berries (-10% risk) and to drink more coffee (-38% risk; Virtanen. 2011). If you are afraid that your offspring may be too small, you better eat fruit and veggies instead of pills, as the consumption of the former and not the total amount of micronutrients correlates with the size of a newborn (Loy. 2011). Thusly avoiding low intakes of (leafy) vegetables and (malaceous) fruits, all you need to reduce the incidence of allergic wheeze in your offspring is to make sure you get enough chocolate (low chocolate consumption = +36% increase; Erkkola. 2012) and avoid fruit and berry juices (+40% risk increase) and and you should be good to go ;-)

The overall message should yet be: Don't stuff or starve yourself and stick to the principles of healthy living I have been trying to piece together like a puzzle in the past 727 posts and the countless comments here at the SuppVersity. This will be good for you and for your offspring!

In the last decade more and more scientists have tried to elucidate the exact mechanisms behind this metabolic deteriorations. And while the increased awareness of the importance of dietary folate is probably the most prominent results of these efforts, vitamin B9 is by far not the only (micro-)nutrient in your diet which can exert far-reaching long-term effects on your offspring. And though much of the information we have is based on rodent or epidemiological human data, I believe that it is worth considering how what you eat today, may influence the health of your children in the future:

• Micronutrient deficiency and body fat % of the offspring: In a series of studies, Rao et al. were able to show that total (-50%) micronutrient deficiency, as well as an insufficient supply of magnesium, manganese, chromium, zinc, folic acid or vitamin B12 (summary in Rao. 2012) led to statistically significant increases in body fat levels in the offspring of rats. And while the effects of maternal chromium and manganese deficiency could be corrected later in life, those that were induced by a lack magnesium, zinc and vitamin A (Ribot. 2001) in the diet of the pregnant rat dams, were permanent.
   
• Exaggerated cortisol release due to high fat diet and insufficient chromium: Both a diet insufficient in the trace element chromium (Padmavathi. 2010), as well as one of the standard "high fat diets" (30% fat; 16% protein; 37% carbs; Bullo-Cioca. 2010) increased the corticosteroid (cortisol) response to stress and thusly increased the diabetes and obesity risk of the offspring of chromium deficient or HFD significantly. Unpublished results by Roa et al. suggest that a similar increase in 11-beta-HSD (the enzyme responsible for the formation of cortisol) exist for folate and vitamin B12, as well (Rao. 2012).
   
• Cholesterol, triglycerides and other lipids: While an insufficient intake of manganese during pregnancy appears to make the offspring more susceptible to diabetes, obesity and low-grade inflammation, a profound lack of magnesium and zinc reduced the levels of cholesterol and cholesterol and triglycerides, respectively (Venu. 2008; Padmavathi. 2009).
   
• Iron deficiency results in growth retardation and brain chemistry: Pubs born to rats on an iron-deficient diet were not only smaller and had altered lipid metabolisms, they also exhibited disturbances in brain dopamine metabolism and defects in the brain myelin (fatty layer that protects the neurons) fatty acid composition (Kwik-Uribe. 2000)
   
• Reduced and exaggerated salt intake predispose to hypertension: As of late the FDA has been going back on their recommendation to avoid salt like a plague and while their reasoning was a different one, the results of a 2011 study by Kaleganova et al. confirm that both a high and a low sodium intake during pregnancy can lead to pathological changes in the kidney morpholgy of the offspring and, subsequently, to hypertension (Kaleganova. 2011)
   
• Increased susceptibility to obesity in response to high-dose multi-vitamin supplementation: Although the overall message of the above effects of nutrient-depended epigenetic programming appears to be that you better make sure not to be deficient in any nutrient, the results of a 2009 study by scientists from the University of Toronto (Szeto. 2009), suggests doubling your already high-dose multivitamin "just to make sure", is probably the worst "prophylactic" measure you could resort to. After all the pubs that were born to rats who received the high dose (10x RDA) vitamin supplement in the Szeto study, were profoundly insulin resistance, hyperphagic and obese.

While some of these negative consequences of maternal and subsequent fetal mal-nutrishment are either reversible (by replenishing respective nutrients) or induced by developmental changes and consequent malfunction of organs or organ systems, it becomes increasingly clear that some of the changes are of epigenetic nature, which means that certain DNA strains are activated or deactivated via methylation in response to dietary restrictions or, as in the case of overall malnurishment or the so-called "high fat diet", an under-, respectively overabundance of energy.

Protein (mal-)nutrition during pregnancy and epigenetic consequences

Image 3: The effects of protein malnutrition on pediatric health are profound, at any age!

Of the macronutrients, dietary protein appears to exert the most profound epigenetic effects during the fetal period. The offspring of protein malnurished rats in a 2005 study from the University of Southhampton in the UK (Lillycrop. 2005), for example, had ~20% lower PPAR-alpha and glucocorticoid receptor methylation status than that of rats on a protein sufficient diet. The subsequent >10x higher PPAR-gamma and 2x higher glucocorticoid receptor mRNA expression render provide a "mechanistical" (obviously it is a physiological one, but if we think of the body as a epigenetically controlled machine, the expression "mechanistic" would be adequate) explanation for the increased susceptibility to dietary induced obesity in later life - an effect, by the way, which has only recently been shown to be sex-depended and more pronounced in female than male offspring of mice (van Straten. 2012).

A high protein content of an overall energy deficient diet, on the other hand, has recently been shown to correct the increased cardiovascular disease risk subsequent to fetal malnutrition in mouse offspring (Kavamura. 2012), which could in fact be related to a correction, or rather aversion of the detoriations in glucocorticoid receptor expression observed in the Lillycrop study (see above).

Note: A 2011 study from the Department of Nutritional Sciences at the University of Toronto suggests that even though soy may be less of a problem for women than men, you would be ill-advised to eat (or feed your pregnant wife) larger amounts of soy protein. After all, the scientists comparison of soy vs. casein based diets showed that the offspring of the soy-fed rodents exhibited increased body and fat pad weights and a statistically highly significant increase in systolic blood pressure - an effect that was, in this case, more pronounced in the male, than in the female pubs (Jahan-Milan. 2011).

Interestingly, we see very different effects with postnatal protein restrictions, only recently, a group of researchers from the Universidade do Estado do Rio de Janeiro, in Rio de Janeiro, Brazil (Lisboa. 2012), that the offspring of the dams received a low protein (8% vs. 23%) diet during the lactation period had lower adipocytes area, a higher leptin:visceral fat ratio, increased leptin receptor expression (and thusly sensitivity) and significantly higher levels of thyroid hormones (T3 and T4) at lower TSH levels than the adult offspring of mothers who had received the normal diet during lactation. These results emphasize the need for further research and confirm my repeatedly voiced concern about jumping to radical conclusions. After all, the same high protein diet that could decrease the CVD risk of your children could be one of a myriad of factors which contribute to the rampant rise of thyroid problems, these days.

Don't surrender, and outdo your well-meaning parents

If coupled with prenatal stress exposure, which has also been shown to induce profound negative effects on the glucocorticoid metabolism of the offspring (Brunton. 2010), protein malnutrition could form a "duo infernale", which would verify the initial statement that some people have an "epigenetic disadvantage" compared to others. It would yet be unfair and above all unproductive to lay the blame on your parents. After all, familial studies suggest that only 30%-50% of the weight gain could potentially be explained by (epi-)genetic factors (Lawin. 2009). This leaves a huge margin for you to intervene and still emphasizes the importance of watching your own diet - for your own, and the sake of your children and grandchildren (I guess, we forget about humanity for now ;-)

High Protein Diets, Acid Load, Calcium Loss, Osteoporosis and a 50% Increase in Diabetes Risk - Is There a Link?

Shouldn't it be obvious that the "happy medium" must be the solution, when high protein leads to brittle bones, and low protein to frail muscle? Sure! But where is this "happy medium"?

Some of you may remember my recent Facebook post "High Protein Diet in the Firing Line. Rodent Study Says: Kidneys Are at Risk". It was based on a press release you could read on all the major science-news outlets on the Internet; a press release that will give the average reader the impression that the corresponding study by Aparicio et al. would "prove" that high protein diets will ruin your kidneys and eventually jeopardize your health (read more).

Another paper (Cao. 2014), Jose Antonio, the CEO of the ISSN and the editor of the ISSN's journal posted on Facebook yesterday, didn't get as much media attention, though.

No wonder, the message of this study is after all not in line with one of the fundamental arguments you will hear, whenever you question the allegedly necessary restriction of total protein intake to 0.8g/kg, maximally 1.2g/kg protein per kilogram body weight day in the current nutritional guidelines:

"[...S]hort-term consumption of high-protein diets does not disrupt calcium homeostasis and is not detrimental to skeletal integrity."

That's not what you will learn at med-school and it is certainly not in line with the hysteria about protein intakes that are 2x or even 3x higher than the 0.8g protein per kilogram body weight we are supposed to consume. Apropos RDA, the subjects in the control group of the said study by Jay J Cao et al. consumed a diet that contained exactly those 0.8g/kg body weight that's supposed to be good for us. The 21 human guinea pigs in the treatment groups, on the other hand, consumed 2x and 3x more than the average dietitian would recommend and they did so for 31 days (Cao. 2014).

Figure 1: Protein intake (in g/day; left), mineral intake (in mg/day; middle)  and calculated renal acid load (in mEq; right) of 49 normal weight, healthy men (n=32) and women (n=7) who consumed normal (0.8g/day), high (1.6g/kg per day) and very high protein (2.4g/kg per day) energy restricted (40%) diets for 4 weeks (Cao 2014)

If you take a look at the PRAL values in Figure 1, you can see that math (not bio- or physiology!) tells us that this reckless practice could compromises the acid-base balance of the healthy, normal-weight subjects, whose energy restricted diets were modeled on the increasingly popular high protein weight loss diets.

Equations vs. experiments | PRAL vs. urinary calclium loss | theory vs. practive

The urinary analysis the scientists conducted does yet speak a very different language. There is, as the scientists emphasize in the discussion of the results no evidence that

Suppversity Suggested Read: "High protein diet = high protein loss" | more

"habitual consumption of dietary protein at levels above the RDA [would] significantly alter urinary calcium excretion, dietary calcium retention, or markers of bone turnover or BMD, despite increased urinary acidity. These results indicate that diets that are 2 or 3 times the RDA for protein are not detrimental to calcium homeostasis when calcium and vitamin D are consumed at recommended intake"

In that I would like to emphasis the importance of adequate calcium (min. 800mg/day) and vitamin D intakes (800-1000IU/day) and the fallacy of the word "habitual". The study at hand did not test the effects of "habitual" high protein consumption. It tested the effects of short-term (28 days) high protein consumption in a low calorie scenario, which is by definition less prone to produce adverse inflammatory and thus potentially pro-osteoporotic side effects (Mundy. 2007).

Not eating enough protein could increase bone loss, when you're dieting

In view of the fact that the evidence I am about to cite, stems from rodent model of postmenopausal bone metabolism, I deliberately used the word could in the headline of this paragraph. And still, the way in which the low protein diet  "negatively impacted bone mass and magnified the detrimental effects of vitD and/or estrogen deficiencies" (Marotte. 2013) in the pertinent study from the Buenos Aires University is particularly disturbing.

High dietary acid load increases diabetes risk by more than 50%: In spite of the fact that this is neither bone- nor kidney-specific, the 56% increase in diabetes risk scientists from the Gustave Roussy Institute in France report in their latest paper in Diabetology, for the 16,621 subjects with PRAL values of only 7 mEq/day is so impressive that I simply had to include it in this article. Specifically in view of the fact that a brief glimpse at the food intake of the subjects in the figure to the left will suffice to see that protein is by no means the only "acid" offender in the SAD diet.

The (postmenopausal) women the scientists try to model with their ovariectomized rats (=rats whose ovaries have been removes) are after all one of the many patient groups who are advised to carefully control their protein intake to make sure that the additional acid load will not compromise their bone health even further and that in spite of the fact that there is ample evidence that the current RDA for protein is inadequate to maintain optimal health, particularly when the total energy intake is restricted and especially in populations who are susceptible to bone loss (Kerstetter. 2005; Chernoff. 2004).

Figure 2: We know for quite some time not that low protein diets decrease the absorp- tion of protein (Kerstteter. 2005). It's not certain if this is "just" a homeastatic me- chanism to stabilize the net/acid balance.

In their 2005 study, Kerstetter et al. were in fact able to show that protein intakes that are 2.6x higher than the RDA increase the effective absorption of calcium from the diet (see Figure 2).

This increase stands in contrast to the significant decrease in calcium absorption the researchers observed in the healthy young (age: 26y) women in the low protein arm (0.7g protein per kg body weight) of the study and should remind us that a reduction in protein intake is not going to stop the insidious loss of bone that's caused by the triage of low estrogen, no exercise and a diet that may be low in protein, but high in acid producing grains (Remer. 1995) and devoid of alkaline fruit and vegetables.

I could now go more into details, but I will just leave you with the notion that the "paleo diet" is, despite its high meat content, among the most kidney-, and above all bone-friendly diets we know. In fact, its fruit and vegetables content yield a net alkaline renal load, and will lead to significant improvements in urinary calcium excretion rates (Appelet. 1997; Frassetto. 2013).   

☄ Note: If you want more about the "Paleo connection" - let me know this (best on Facebook) and what you would be most interested in and I will address that in a future SuppVersity article.

Practically speaking: The results of the Cao study tell us that you can get away with a high protein load in otherwise SAD-ly (SAD = standard American diet) normal diet in the short run. What it does not tell you is that you can keep on this kind of "just add a ton of protein to the regular junk you eat diet" with ever-increasing dietary acid loads won't hurt your kidneys, bones and pancreas (see red box) in the long run.

If you want to eat a high protein diet, that's free of kidney, bone, or general meta- bolic side effects, it will thus have to have the fruit and vegetable content of what we currently deem a "paleo diet" - a diet with a relatively high protein content, tons of vege- tables, tubers and fruit and a limited (not no!) amount of grains. This will bring your citrate, magnesium and potas- sium intake up spare calcium and help you to ward off the evermore prevalent diabesity epidemic.

Bottom line: It may be human, but still is idiotic to isolate any single macronutrient as "the reason" for osteoporosis and bone loss. Looking exclusively at what we could potentially be doing wrong is not going to help us here. Rather than that, we should look at what we can be doing right - in other words, what should we eat, if we want to maintain not just bone-, kindey-health, but also muscle- and metabolic health (note: protein alone won't help you maintain muscle mass).

If we look at the results of the previously referenced trial by Frasetto et al., in which the researchers from the University of California San Francisco, which achieved a reduction of the potential renal acid load from 28mEq (which is more than the PRAL of 7mEq that's associated with a >50% diabetes risk; see red box) to -96 mEq on a diets that differed not in macronutrient, but in food, and consequently micronutrient-, specifically mineral-content, you will be hard pressed to keep the deabte on the short-sighted  "carbohydrates are good, protein is bad and fat is the devil, anyways"-level it is currently on.

We should be talking about food, instead. Not just about "more fruit and vegetables", but also about what you will necessarily have to skip for them, if you want your diet to work: Highly processed foods, including meats(!), sodas and other sweetened drinks, white bread, candy, chips, etc. It's not that you can't ever eat any of those, but as long as any of these items is on your list of foods you eat on a daily basis, there is still room for improvement.

References

• Aparicio, V. A., et al. "High-protein diets and renal status in rats." Nutrición hospitalaria: Organo oficial de la Sociedad española de nutrición parenteral y enteral 28.1 (2013): 232-237.
• Appel, Lawrence J., et al. "A clinical trial of the effects of dietary patterns on blood pressure." New England Journal of Medicine 336.16 (1997): 1117-1124. 
• Cao, Jay J., et al. "Calcium homeostasis and bone metabolic responses to high-protein diets during energy deficit in healthy young adults: a randomized controlled trial." The American journal of clinical nutrition 99.2 (2014): 400-407.
• Chernoff, Ronni. "Protein and older adults." Journal of the American College of Nutrition 23.sup6 (2004): 627S-630S. 
• Frassetto, L. A., et al. "Established dietary estimates of net acid production do not predict measured net acid excretion in patients with Type 2 diabetes on Paleolithic–Hunter–Gatherer-type diets." European journal of clinical nutrition 67.9 (2013): 899-903.
• Kerstetter, Jane E., et al. "The impact of dietary protein on calcium absorption and kinetic measures of bone turnover in women." Journal of Clinical Endocrinology & Metabolism 90.1 (2005): 26-31.
• Mundy, Gregory R. "Osteoporosis and inflammation." Nutrition reviews 65.s3 (2007): S147-S151.
• Remer, Thomas, and Friedrich Manz. "Potential renal acid load of foods and its influence on urine pH." Journal of the American Dietetic Association 95.7 (1995): 791-797.

High Fructose Consumption, Inflammation Up, LDL/HDL Ratio Down - Is That Good or Bad For Your Heart?

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.

Learn more about fructose at the SuppVersity

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

Fructose From Fruit is NOT the Problem

Americans Don't Eat More Fructose These Days!

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

Fructose is Not Worse Than Sugar

The Obesogenic Fructose Fat Connection

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).

Apples reduce, apple juice increases hs-CRP in healthy volunteers (Ravn-Haren. 2013).

Don't mistake fruits for pure fructose: Studies indicate that a high fruit consumption is associated with reduced hs-CRP scores and a lower mRNA expression in peripheral blood mononuclear cells of some relevant proinflammatory gene markers (Oliveira. 2009; Hermsdorff. 2010). This is yet not the case for fruit juices, as you may remember from a previous SuppVersity post discussing the results of Gitte Ravn-Haren's 2013 study which showed that the intake of whole apples had beneficial, the consumption of apple juice, however, detrimental effects on plasma lipids and - as you can see in the figure to the left - hs-CRP levels of the healthy volunteers (Gitte Ravn-Haren 2013).

Well, yes, but (a) it's 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). That's not ana optimal level, but considering the fact that we are talking about "average Joes and Janes" who probably don't 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) that's 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. That's 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 wasn't in the danger zone before, either.

Incremental area under the curve for glucose and insulin 0-120min after consuming the test beverages (Jameel. 2014).

So what? Overall the results provide no evidence that the occasional consumption of a larg(er) bolus of fructose was unhealthier than the same amount of glucose or sucrose. If you take a parting look at the glucose and insulin response you will also see why fructose has long been haled as the "healthier" alternative to sugar for type II diabetics: there is no increase in glucose or insulin in response to the ingestion of 50g of fructose. And even the dreaded increase in triglycerides that occurs when the liver converts the fructose to fat did not occur (in fact, the levels dropped by ~4%, while they increased when the subjects consumed glucose (+11%) or sucrose (+4%).

So, if you've been drinking your first real coke of 2015 last night, don't worry. It probably didn't hurt your heart. If you plan to continue drinking 1l of the brown sugar-liquid everyday, this year, though, I would not guarantee that the extra pounds you may be gaining and the diabetes you may be developing won't have negative consequences for your heart and maybe liver health  | Comment on Facebook.

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.