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Some butter on top of the broccoli would allow for the assimilation of the absorption of the 101.6?g vitamin K 623IU vitamin A (various).

There are a handful of very basic questions in nutrition science, no one appears to have an answer to. One of these questions, which is directly related to the  well-known fact that the vitamins A, D, E & K are "lipid soluble". This means that they are "solved" and thus made absorbable by fats and oils. The general assumption is thus that the vitamins A, i.e. the retinol and carotenoids, all forms of vitamin D, the tocopherols and -trienols (vitamins E) and the two major forms of vitamin K, i.e. phylloquinone (K1) and menaquinone (K2) will only be absorbed, if you consume them with a sufficient amount of dietary fat. Now, the questions obviously are (a) is this correct and (b) how much is sufficient.
In view of the fact that the answers to (a) and be are not necessarily identical for all four vitamins of interest, it appears sensible to tackle them one after the other.


Starting with vitamin A and the various forms of carotenoids, we can already confirm that (a), i.e. the assumption that we need dietary fats to optimally absorb vitamin A is correct. As Karin van het Hof and her colleagues point out, the "amount of dietary fat required to ensure carotenoid absorption [does yet] seem low (?3–5 g per meal), although it depends on the physicochemical characteristics of the carotenoids ingested." (van het Hof. 2000) In spite of the fact that 5g of fat are not exactly much, the classic uncooked vegetarian orthorexic salad often comes with a total of only 5g of fat of which 95% remain at the bottom of the salad bowl. If that sounds like your favorite dish, you should be aware that you are risking that all the good  beta- and other carotenoids in the salad will pass right through.

Figure 1: Changes in hepatic vitamin A (retinol) and carotenoid stores in gerbils after 14 days on high fat (30%) vs. low fat (10%) diet (Deming. 2000)

In that, the concomitant presence of both dietary fat and carotenoids in a meal is a necessary prerequisite for the absorption of vitamin A, also because the fatty acids will trigger the conversion of of beta-carotene into vitamin A and its subsequent absorption via the lymphatic system (Ribaya?Mercado. 2002). It is thus not surprising that animal studies by Lakshman et al. (1996) and Deming et al. (2000; see Figure 1) suggest that low fat diet can lead to a depletion of the vitamin A tissue stores even if the serum levels remain constant. The amount of fiber in the diet, on the other, has no influence the absorption of vitamin A (Mills. 2009).

Interestingly enough, the provision of the fat blocker Orlistat reduces the absorption of vitamin A only insignificantly, as a 1996 paper by Angela T. Melia, Susan G. Koss?Twardy, and Jianguo Zhi would suggest (Melia. 1996).

Which takes us right to vitamin E, the absoprtion which is - in spite of being "blocked" by the fat blocker orlistat (Melia. 1996) - less susceptible to the absence of dietary fat than you may think. Annet JC Roodenburg, Rianne Leenen, Karin H van het Hof,  Jan A Weststrate, and Lilian BM Tijburg do in fact argue that the optimal intake of vitamin E requires only "a limited amount" of dietary fat (Roodenburg. 2000).

Figure 2: Vitamin E serum levels after 7 days on control (low fat, 3g) or high(er) fat (36g) diet with and without supplemental vitamin E (Roodenburg. 2000)

As you can see in Figure 2. A minimum intake of only 3g per day was sufficient to keep the vitamin E levels stable. The short study period of 7-days (each) and the absence of measures of tissue concentration of vitamin E do yet reduce the practical relevance of the data, Roodenburg et al. present in their Y2k paper in the American Journal of Clinical Nutrition.
If you take a look at the high prevalence of vitamin E dieficiency among the fat (and PUFA) "loving", or at least eating, majority of Americans, it does yet become obvious that a lack of dietary fat is not just theoretically, but also practically not exactly the #1 reason you may become deficient in tocopherols and -trienols. That the latter is an increased demand due to chronic inflammation and the (over-)consumption of exactly those PUFAs that come with a shitload of vitamin E in nature, for a reason would yet be a topic for another SuppVersity article and thus something we will skip to fast forward to ...

...Vitamin K, obviously. Vitamin K is a relative newcomer to the publics understanding of the alphabet soup. Aside from being it a good tool to rip customers vitamin K, or rather K1 (plant sources) and K2 (animal sources) are thus also the only fat soluble vitamins not everyone knows. The fact that the amount of phylloquinone (K1) that makes it into your blood stream is ~70% reduced if you eat your spinach without fat (Gijsbers. 1996).

And if we take the results researchers from the Gifu University School of Medicine present in a 1996 paper in the Journal of Pharmacological Sciences, as a reference, the amount of fat you need to optimally absorb your K2 (menaquinones), is not exactly low.

Figure 3: For optimal absorption of K2, there has got to be a huge amount of fat in the meal - but who wonders. K2 comes with a high amount of fat (Uematsu. 1996)

Uematsu et al. had to supply their subjects, who consumed otherwise identical test meals with 8.8, 20.0 and 34.9g of fat in them with the maximal (i.e. 35g) of fat before the K2 absorption maxed out. In that the total area under the curve did not really differ between those subjects who consumed the K2 before and those who took it immediately after the test meal.

Thats a pity, cause a high intake of vitamin K (menaquinone from animal sources) has been associated with a 27% reduced risk of developing heart disease (Geleijnse. 2004), an ailment of which many still believe that it was brought about by the fat they need to optimally absorb their vitamin K.

For vitamin D, our last "V" on the list, things look differently. For one, everybody knows about this miracle vitamin and for two, it may be "fat soluble", but the amount of fat thats required to optimally absorb it turned out to be much lower than previously thought (see "A Fat D-Ficiency! Do You Really Need More Vitamin D or Simply More Fatty Foods? Study Shows, Even 50.000 IU of Vitamin D3 Useless, When You Ingest It Without Fat. " | read more).
In fact, Niramitmahapanya et al. found in 2011 that its not necessarily a high amount, but rather the right type of fat that determines if and how much of the vitamin D you take in capsule form or find in comparably low amounts in your foods that determines how much of the vitamin D actually makes it into your bloodstream:

"The change in plasma 25OHD (nanograms per milliliter) during vitamin D supplementation was positively associated with MUFA, (? = 0.94; P = 0.016), negatively associated with PUFA, (? = ?0.93; P = 0.038), and positively associated with the MUFA/PUFA ratio (? = 6.46; P = 0.014)."

In plain English this means, that the "good" seed and vegetable oils with their high PUFA content will effectively inhibit the absorption of vitamin D - an observation that adds to the many reasons the modern sedentary, sun-avoiding, sun-screen using, soybean oil (MUFA:PUFA = 0.4) guzzling American is low in or  quasi devoid of vitamin D.

Figure 4: 25(OH)D levels of 30 healthy men and women after ingestion of 50.000IU vitamin D3 supplement in conjunction with a normal or low fat breakfast (Raimundo. 2011)

Against that background its not surprising that you will not find a conclusive answer to the question how much fat you actually need. In a study that used a fatty meal with soybean oil in it, the effect would be totally different from one in which the subjects consumed meals that were made with sunflower oil, an oil with a MUFA:PUFA ratio >1. In view of the results Gnadinger et al present in a recent appear it does still seem appropriate to consume at least some fat alongside your vitamin D supplements. As far as the food-borne vitamin D is concerned, you dont have to worry, anyways. Foods that are high in D3 usually come with all the fat you need to absorb it.

How much fat, exactly you would need to make the most of dietary and supplemental vitamin D, on the other hand, is still not known. The previously mentioned data from the study by Raimondo et al. (see Figure 4, to the right) I wrote about in "A Fat D-Ficiency" is obviously still valid. The extremely high amount of vitamin D (50,000IU!) could yet require a correspondingly high amount of fat to be optimally absorbed and the fact that the fat in the study came from a "vegetable margarine" with an undisclosed ratio of MUFA:PUFA does not make the real-world effects any more predictable.
References:

• Chitchumroonchokchai, Chureeporn, et al. "Dietary fats with increased ratio of unsaturated to saturated fatty acids enhance absorption of carotenoid and vitamin E by increasing both efficiency of micellarization and lipoprotein secretion." FASEB J 24 (2010): 539-3.
• Deming, Denise M., et al. "Amount of dietary fat and type of soluble fiber independently modulate postabsorptive conversion of ?-carotene to vitamin A in Mongolian gerbils." The Journal of nutrition 130.11 (2000): 2789-2796. 
• Geleijnse, Johanna M., et al. "Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study." The Journal of nutrition 134.11 (2004): 3100-3105.
• Gijsbers, Birgit LMG, Kon-Siong G. Jie, and Cees Vermeer. "Effect of food composition on vitamin K absorption in human volunteers." British Journal of Nutrition 76.02 (1996): 223-229.
• Goodman, Dew S., et al. "The intestinal absorption and metabolism of vitamin A and beta-carotene in man." Journal of Clinical Investigation 45.10 (1966): 1615.
• Jayarajan, P., Vinodini Reddy, and M. Mohanram. "Effect of dietary fat on absorption of ? carotene from green leafy vegetables in children." Indian journal of medical research 137.5 (2013).
• Kris-Etherton, P. M., et al. "Polyunsaturated fatty acids in the food chain in the United States." The American journal of clinical nutrition 71.1 (2000): 179S-188S.
• Lakshman, M. R., et al. "The effects of dietary taurocholate, fat, protein, and carbohydrate on the distribution and fate of dietary ??carotene in ferrets." (1996): 49-61.
• Melia, Angela T., Susan G. Koss?Twardy, and Jianguo Zhi. "The effect of orlistat, an inhibitor of dietary fat absorption, on the absorption of vitamins A and E in healthy volunteers." The Journal of Clinical Pharmacology 36.7 (1996): 647-653.
• van het Hof, Karin H., et al. "Dietary factors that affect the bioavailability of carotenoids." The Journal of nutrition 130.3 (2000): 503-506.
• Raimundo, Fabiana Viegas, et al. "Effect of high-versus low-fat meal on serum 25-hydroxyvitamin D levels after a single oral dose of vitamin D: a single-blind, parallel, randomized trial." International journal of endocrinology 2011 (2011).
• Ribaya?Mercado, Judy D. "Influence of Dietary Fat on ??Carotene Absorption and Bioconversion into Vitamin A." Nutrition reviews 60.4 (2002): 104-110.
• Roodenburg, Annet JC, et al. "Amount of fat in the diet affects bioavailability of lutein esters but not of ?-carotene, ?-carotene, and vitamin E in humans." The American journal of clinical nutrition 71.5 (2000): 1187-1193. 
• Uematsu, Toshihiko, et al. "Effect of dietary fat content on oral bioavailability of menatetrenone in humans." Journal of pharmaceutical sciences 85.9 (1996): 1012-1016.

PENTAX has long made an excellent digital SLR that offers excellent image quality and an intuitive interface. PENTAX KR is a 12 megapixel SLR camera with 15-55 mm lens. This digital camera is also very compact, lightweight, but very sturdy.


As with most SLR cameras, KR is a compact and lightweight so easy to carry all day. A good grip design makes PENTAX KR is very comfortable when held. This digital SLR also feels very sturdy with bbot 21 ounces with batteries and memory card

PENTAX has always made simple interface, as well as KR. A single mode button on top gives you quick access to change from manual to automatic and scene modes.

Settings and camera status displayed on the LCD screen of 3 inches. While the LCD screen has a menu that is organized, the menu is not automatically turned off when you lift the camera and saw the object through the optical viewfinder. PENTAX KR using the sensor is stable, which means any lens you use will receive a benefit in stability.


Features


PENTAX KR has an excellent set of features, this camera has a higher ISO (12800, expandable up to 25 600) and a larger screen and high resolution. KR was able to shoot more frames per second in shooting mode continuously (6fps) and has a number of new effects, such as HDR and Cross Process.

PENTAX has brought PRIME II image processor is the same just as the K7 and KX KR and this makes it very fast. Wakti boot, save images and menu navigation are all very quick and responsive.

Sensor cleaning is a feature that will show you the dust on the sensor. Live View is provided to use the LCD screen as a viewfinder. PENTAX KR can record HD video at 24fps 72p including mono microphone. Like most SLR cameras, video shooting with KR requires skill and expertise due to lack of autofocus.

PENTAX K-R Specifications


Sensor Size and Type: 23.6 x 15.8mm. CMOS with primary color filter and integrated Shake / Dust Reduction sensor movement system-
Max. Image Resolution: 12.4 Megapixel
ISO Sensitivity: Auto: 200-12800 (1, 1/2, 1/3 EV steps), up to 1600 in Bulb
Built-in Flash: Retractable P-TTL auto / manual popup flash Guide number: 12 (100 / m), 16 (200 / m) Coverage: 28mm wide angle (equivalent to 35mm).
Auto Focus: TTL phase-matching 11 points (9 cross) wide autofocus system (SAFOX IX) Focus modes.
LCD Monitor: 3.0? TFT LCD color monitor adjustable w
External Flash: Hot shoe (P-TTL, high speed sync)

see video:

It was about time for an artificial sweetener update, wasnt it?

Alright, I have to admit I am not following the artificial sweetener scene closely enough to have heard about SUCRAM, an artificial sweetener that is composed of saccharin (a classic) and neohepseridin dihydrochalcone, the new kid on the blog, which is yet not officially approved by either the FDA or it European equivalent o be used in the processed junk, most people call "food", these days. If we put some faith into the latest study investigating the effects of this agent, which is apparently already heavily used in animal feeds in Europe it does yet "dramatically reduce enteric disease" and "enhance growth performance in early-weaned piglets." (Daly. 2014)

Whether and to which extent these beneficial effects on gut health are mediated by changes in the gut microbiome is yet still uncertain; and since "uncertain" is a word scientists dont like, Kristian Daily and his colleagues from the University of Liverpool conducted a study to find out, whether the non-negligible health benefits would be brought about by AI <> gut interactions.
To this ends, the scientists employed a DNA-based pyrosequencing technology to investigate the changes in the intestinal microbiota of piglets weaned to a diet supplemented with either a natural sugar, lactose or said artificial sweetener (SUCRAM)

Figure 1: Total and lactobacillus OTU4228 concentrations in piglets on hydrolzysate carbohydrate diet without sweeteners, with lactose or SUCRAM diets and corresponding concentration of lactic acid in the caecal contents (Daly. 2014)

As you can see in Figure 1, both, the addition of lactose and the saccharin/NHDC mix lead to dramatical increases in the caecal Lactobacillus population and could well explain the previously reported "pro gut health" effect of SUCRAM in piglets (Vente-Spreeuwenberg. 2004; Pierce. 2006)

But thats obviously not all thats news-worthy!

I did after all promise you news on products you may be using, as well - aspartame and acesulfame-k, to be precise. Now, while the former is a constant target of public (mostly broscientific) criticism, the latter has been a thorn in my side ever since I have started investigating artificial sweeteners.

Lean more about the "Gut Type Diet" - No Fad, Guaranteed!

And while previous studies only suggested that the effects of acesulfam-k on the pancreas could have pro-obesogenic consequences, a recent model experiment from the Louisiana State University appears to finally prove that acesulfam-k may actively promote the deposition of body fat in the presence of insulin resistance.

Ok, the results have been derived in a Caenorhabditis elegans, a "worm", but one that has long and actually surprisingly successfully been used as a "model for studying the basic biology of obesity" (Jones. 2009) - I know, I am not convinced either, but if the results do actually translate to humans, this would be major (bad) news for the food industry.

In view of the fact that most companies have been pulling acesulfame-k from their products over the past years, anyway, I would not discard the findings Jolene Zheng et al. present in their latest paper in Chemico-Biological Interactions as meaningless, not despite, but rather because a scientists from PepsiCo was part of the research team which observed these significant increases in intestinal fat (=visceral fat of the worm) when the critters were fed with acesulfam-k sweetened coke.
References: 

• Payne, A. N., C. Chassard, and C. Lacroix. "Gut microbial adaptation to dietary consumption of fructose, artificial sweeteners and sugar alcohols: implications for host–microbe interactions contributing to obesity." Obesity Reviews 13.9 (2012): 799-809.
• Pierce, K. M., et al. "The effect of lactose and inulin on intestinal morphology, selected microbial populations and volatile fatty acid concentrations in the gastro-intestinal tract of the weanling pig." ANIMAL SCIENCE-GLASGOW THEN PENICUIK- 82.3 (2006): 311.
• Jones, Kevin T., and Kaveh Ashrafi. "Caenorhabditis elegans as an emerging model for studying the basic biology of obesity." Disease models & mechanisms 2.5-6 (2009): 224-229.
• Vente-Spreeuwenberg, M. A. M., et al. "Effect of dietary protein source on feed intake and small intestinal morphology in newly weaned piglets." Livestock Production Science 86.1 (2004): 169-177.