Study Suggests: Frozen Veggies Worse Than Common Wisdom Says - Frozen Asparagus, Zucchini and Green Beans Lose More Antioxidants During Boiling

Green asparagus from the fridge and  from the market are not created equal - at least not when they finally end up on your plate after a short bath in hot water.

You just have to watch one of the consumer report shows on television to hear it: "Frozen veggies are way better than their reputation would suggest." Actually, here in Germany this sentence has been repeated to soften that I've even heard people say they'd buy the frozen broccoli because it contained "more vitamins and the other good stuff, you know." And you know what? For some veggies like spinach, for example, this may actually be the case. For others, like broccoli or peas, the nutrient status of the frozen and the raw uncooked vegetable appears to be more or less identical (Favell. 1998). But that's something you cannot say for the green asparagus stems, zucchini and green beans in a recent study from the Università degli Studi di Parma in Italy.

Warning: Don't take this article as an excuse and stop eating veggies completely. The frozen stuff may lose more vitamins, when you boil it, but (a) you can still blanch it and (b) even with significantly reduced antioxidant effects veggies are still among the healthiest things you can eat.

I am not an asparagus expert and can still tell that the cell structure of the Transverse  sections boiled (C - from raw | D - from frozen) is profoundly messed up compared to the raw (A) and blanched (B) variety | legend: c = collenchyma; vp = vascular bundle; p = parenchyma; f = fissure.

In the corresponding experiment, the Italian researchers bought Green asparagus stems (Asparagus officinalis L., var. Grande), zucchini (Cucurbita pepo L., va Quine) and green beans (Phaseolus vulgaris L., var. Giamaica) from a local producer and processed them within 24 hours from harvesting. For each of the veggies four samples were prepared: Raw/uncooked  (R), raw/boiled  (B), blanched (BL) and industrially frozen/boiled (FB)

The raw (ten kilograms of each vegetable), blanched (five kilograms of each vegetable) and industrially frozen  samples  (five  kilograms  of  each  vegetable) had been transported were  transported  to  the  University of  Parma laboratories  under  adequate  refrigerated conditions to avoid the exuberant nutrient loss that occurs upon inadequately slow (re-)freezing.

SuppVersity Suggested Read: " Conventional vs. Organic: It's Not About Getting More, But Getting Less For Your Money. Less Pesticides, Dioxins & Co" | read more if you want to know if the claim "organic is always better" is a similar misconcept as "frozen over fresh".

If you "freeze" your veggies in the freezer compartment of your fridge, this will make the cells blast, so that even before they are cooked, and the nutrients flow out. It is generally assume that the latter would not happen, if the veggies are shock-frosted.

Figure 1: Total antioxidant capacity of green asparagus, zucchini and green beans raw, blanched, boiled and frozen and boiled (Paciulli. 2014); as the data tells you frozen veggies with similar  icy grease on them like you see on the right may not really be a better source of antioxidants than fresh veggies from the farmers or even the supermarket.

If we look at the data in Figure 1, though, it would appear that the cells may have "cracked" already so that they are more susceptible to the subsequent heat assault and the frozen + boiled samples end up having consistently lower total antioxidant (Figure 2) and feric acid reducing capacity than their raw + boiled counterparts.

For a similar reason (nutrient retention), the blanched samples have been cooled immediately after blanching in an ice-water bath for 3 min before they have been transported to the laboratories, where their analysis shows that only the Zucchini lost a small, but significant amount of their total antioxidant activity.

Figure 2: It would be interesting to see if the negative effects of freezing and boiling occur in all vegetables. In view of the fact that previous studies compared raw vs. frozen, but nor raw + cooked vs. frozen + cooked, frozen Broccoli + cooked broccoli could be exactly as "bad" as asparagus, zucchini and green beans.

The thing that is of most practical relevance, tough, is the significant negative effect of freezing + boiling on both, the total antioxidant capacity (Figure 1) and the ferric reducing capacity (Figure 2) of all three vegetables.

The previously "cited" statement that you're better of with the "fresh" frozen veggies is thus probably only right, if you eat them raw. Compared to fresh veggies, the previously frozen asparagus, zucchini and green beans lost almost 11-30% of their antioxidant prowess during the cooking process - and the same may well happen to other veggies, including broccoli, which have been compared in previous studies only on a raw vs. frozen, but not on a cooked vs. frozen + cooked basis. Unless you're afraid that all the good veggies may limit your gains due to their potent anti-oxidant effects, it appears smart to stay away from their frozen varieties.

References:

• Paciulli, Maria, et al. "Impact of the industrial freezing process on selected vegetables Part I. Structure, texture and antioxidant capacity." Food Research International (2014).

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 ;-)

Veggies Rule: As an Adjunct to Your Starches Leafy Greens Reduce Postprandial Glycemia + Insulin and Boost the Production of the Anti-Obesogenic Satiety Hormone GLP-1

Don't worry, you don't have to eat veggies only for the rest of your life, but you should never eat a meal without them!

I've been writing about the "add fat to your carbs to ameliorate the obesogenic insulin response" bullsh*t before (see "True or False? Adding Fat to A Carby Meal Lowers Insulin Response. Muscle Hypertrophy Impairs Oxygen Diffusion. Reducing Carb Intake Improve Muscular Insulin Sensitivity" | read more). What I have not been writing about before are better alternatives. Alternatives such as a huge bowl of veggies. A bowl like the one the participants in a recent study from the Graduate School of Human Sciences and Design at the Japan Women’s University in Tokyo consumed as an adjunct to a standardized white rice meal.

Add veggies to your rice!

Basically, the scientists tested four different conditions. In condition (S), the participants consumed only the staple food (boiled white rice weighing 200 g heated in a microwave oven for 2 min). In condition (SM), the participants consumed the staple food (rice) and a main dish, in this case a boiled egg and tofu (soyabean curd). The third condition (SMF) was the same staple bowl of rice and main dish, but this time "enhanced" with an extra serving of fat from delicious mayonnaise.

Table 1: Overview of the composition of the test meals (Kameyama. 2014)

On the last out of four testing occasions, the normal-weight male study participants with an age  between 30 and 49 years consumed the same high fat meal (SMF), but this time with an additional vegetable dish (SMFV) consistinf of boiled spinach and boiled broccoli.

Figure 1: Changes in plasma glucose, insulin, GIP and GLP-1 expressed relative to rice only (Kameyama. 2014)

In view of the fact that I already gave away the results, I don't think the data in Figure 1 requires further interpretation, so let me just tell you this: Your mother was - as always - right, when she told you to eat your veggies - if you still don't understand why, it may be time to read up on the fat burning effects of GLP-1 (spec. "Eat More, Burn More and Lose Fat Like on Crack with GLP-1!?" | read more) and the role of GIP in the production and effects of insulin, here at the SuppVersity.

You want more evidence that veggies are healthy - what about those?

Bottom line: The study at hand provides yet another indisputable argument in favor of having large serving of vegetables with every meal. Contrary to common health-junky believe, the latter must not necessarily be spinach or broccoli. Dark leafy veggies are good, and even if they may not reduce your diabetes risk to the same extend ad leafy green ones do, they won't increase it in the way French fries, pizza and the alibi-salad on an Big Mac do... and I bet, variety - which has AFAIK hitherto not been investigated as a factor in type II diabetes, heart disease or stroke, will figure, as well, anyway.

Reference:

• Carter, Patrice, et al. "Fruit and vegetable intake and incidence of type 2 diabetes mellitus: systematic review and meta-analysis." BMJ: British Medical Journal 341 (2010).
• Dauchet, Luc, et al. "Fruit and vegetable consumption and risk of coronary heart disease: a meta-analysis of cohort studies." The Journal of nutrition 136.10 (2006): 2588-2593.
• He, Feng J., Caryl A. Nowson, and Graham A. MacGregor. "Fruit and vegetable consumption and stroke: meta-analysis of cohort studies." The Lancet 367.9507 (2006): 320-326.
• Kameyama et al. "Effects of consumption of main and side dishes with white rice on
  postprandial glucose, insulin, glucose-dependent insulinotropic polypeptide
  and glucagon-like peptide-1 responses in healthy Japanese men" British Journal of Nutrition (2014): Ahead of print.