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.

The advantage of HDL is its stability that reduces the risk of plaque build-up in the intestinal wall, which is clogged by the remnants of oxidized LDL and causes heart disease & co.

First things first: We are not talking about "hard experimental evidence" as you could generate it in a randomized controlled trial in a metabolic ward. The data I am reporting today is from a cohort with 1,566 participants with extensive lipid phenotype data completed the Harvard Standardized Food Frequency Questionnaire to determine their daily micronutrient intake over the past year - an epidemiological study that used stepwise linear regression was used to separately evaluate the effects of dietary covariates on adjusted levels of HDL-C, HDL-2, HDL-3, and apoA1.

Interestingly, this is the first study with a quality data-set that determined the association between specific dietary micronutrients with HDL-C, HDL-2, HDL-3, and apoA1, and how these dietary associations differ across the various measures of HDL - not just one.
To identify the HDL-promoters in the diet, the scientists use demographic and clinical variables in the base model. What they found was that numerous dietary intakes increased total HDL-C variance.
The results of their stepwise linear regression model in Table 1 indicate - probably for some people much surprisingly - that all alcohol intake levels were positively associated with HDL-C.

"In addition, magnesium, folate, and the saturated fat, myristic acid (14:0), were all positively and independently associated with HDL-C. Carbohydrate intake, iron, and % of fat derived from animal sources were each negatively additive for HDL-C." (Kim. 2014)

Similar effects from dietary intakes were observed for HDL-2, of which we know that it is decreased in women with rheumatoid arthritis (Arts. 2012) and individuals with other inflammatory diseases (including metabolic syndrom) and associated with a slightly higher reduction in acute myocardial infarction risk than "regular" HDL in several studies (Salonen. Salonen. 1991; Stampfer. 1991; Buring. 1992; Gaziano. 1993) for all alcohol intakes, magnesium, folate, and myristic acid (14:0), eicosapentaenoic acid (20:5, a ?-3 EPA), all of which were positively and independently associated with HDL-2 levels.

Table 1:  Best-fit model from stepwise linear regression predicting HDL-C levels using dietary intake data (Kim. 2014)

The opposite was the case for arachidonic acid (20:4, an ?-6 ARA), carbohydrate and iron intakes, which were both negatively associated with HDL-2 (see Table 1).

Dont forget to put things into perspective!

And just to make sure, I dont get angry emails from bulletproof coffee drinkers: Your coffee is fine, the content of the only "good" saturated fat, i.e. myristic acid, happens to be especially high coconut oil (41%; Sodamade. 2013) and relatively high in butter (12% independent of whether its grass-fed or not; Couvreur. 2006) - surprised? Not really, I guess. As a SuppVersity reader you are by now aware that the bad reputation coconut oil and butter have for being mostly saturated fats is no longer supported by contemporary scientific evidence (Dias. 2014).

And with respect to the total animal fat intake - for the average Westerner thats a good measure of how much processed meat he / she eats, so I would not overrate the small negative association (1/80 of the one of having a ton of carbohydrates in your diet!) the scientists found in the study at hand.
References:

• Arts, Elke, et al. "High-density lipoprotein cholesterol subfractions HDL2 and HDL3 are reduced in women with rheumatoid arthritis and may augment the cardiovascular risk of women with RA: a cross-sectional study." Arthritis Res Ther 14.3 (2012): R116.
• Buring, J. E., et al. "Decreased HDL2 and HDL3 cholesterol, Apo AI and Apo A-II, and increased risk of myocardial infarction." Circulation 85.1 (1992): 22-29.
• Couvreur, S., et al. "The linear relationship between the proportion of fresh grass in the cow diet, milk fatty acid composition, and butter properties." Journal of dairy science 89.6 (2006): 1956-1969.
• Dias, C. B., et al. "Saturated fat consumption may not be the main cause of increased blood lipid levels." Medical hypotheses 82.2 (2014): 187-195.
• Gaziano, J. Michael, et al. "Moderate alcohol intake, increased levels of high-density lipoprotein and its subfractions, and decreased risk of myocardial infarction." New England Journal of Medicine 329.25 (1993): 1829-1834. 
• Kim et al. "Effects of dietary components on high-density lipoprotein measures in a cohort of 1,566 participants." Nutrition & Metabolism 2014, 11:44.
• Leon, ARTHUR S., and OTTO A. Sanchez. "Response of blood lipids to exercise training alone or combined with dietary intervention." Medicine and science in sports and exercise 33.6 Suppl (2001): S502-15.
• Salonen, Jukka T., et al. "HDL, HDL2, and HDL3 subfractions, and the risk of acute myocardial infarction. A prospective population study in eastern Finnish men." Circulation 84.1 (1991): 129-139. 
• Sodamade, A¹, and O. S. Bolaji. "Fatty acids composition of three different vegetable oils (soybean oil, groundnut oil and coconut oil) by high-performance liquid chromatography." Chemistry and Materials Research 3.7 (2013): 26-29.
• Stampfer, Meir J., et al. "A prospective study of cholesterol, apolipoproteins, and the risk of myocardial infarction." New England Journal of Medicine 325.6 (1991): 373-381.