What You Don’t Know About Saturated Fat That Could Harm You
By Paul RogersWhat you probably do know is that most dietary recommendations say that you should keep your consumption of saturated fat and cholesterol in food low in order to lower your blood cholesterol and consequently your risk of heart disease.
The usual recommendations are that saturated fat should be no more than 10% of total calories and cholesterol less than 300 milligrams each day – and for people with existing signs of heart disease, less than 7% saturated fat and under 200 milligrams of cholesterol each day.
If you read widely of internet health and nutrition sites, you may also be aware that fringe movements exist that say this is not true; that it’s a government conspiracy and so on, and that saturated fat and cholesterol are as harmless as soft fruit. You can read one of my responses to that. It’s surprising how many otherwise knowledgeable pundits get taken in by this stuff.
What you may not know is that too much saturated fat in the diet has other adverse effects beyond how it raises blood cholesterol. Here is a short summary.
Saturated Fats Cause Dementia
Here is what one research team has to say about saturated (and trans) fat and cognitive function.
“Diets high in fat, especially trans and saturated fats, adversely affect cognition, while those high in fruits, vegetables, cereals, and fish are associated with better cognitive function and lower risk of dementia. While the precise physiologic mechanisms underlying these dietary influences are not completely understood, modulation of brain insulin activity and neuroinflammation likely contribute.” (Ann N Y Acad Sci. 2007 Oct;1114:389-97.)
And another:
“Moderate intake of unsaturated fats at midlife is protective, whereas a moderate intake of saturated fats may increase the risk of dementia and AD, especially among ApoE epsilon4 carriers. “ (Dement Geriatr Cogn Disord. 2006;22(1):99-107. )
Saturated Fats Cause Insulin Resistance
This conclusion provides a pointer to findings from several similar studies:
“A change of the proportions of dietary fatty acids, decreasing saturated fatty acid and increasing monounsaturated fatty acid, improves insulin sensitivity . . . ” (Diabetologia. 2001 Mar;44(3):312-9.)
And:
“Therefore, prevention of the metabolic syndrome has to be targeted . . . and . . . to improve insulin sensitivity and associated metabolic abnormalities through a reduction of dietary saturated fat, partially replaced, when appropriate, by monounsaturated and polyunsaturated fats.” (Clin Nutr. 2004 Aug;23(4):447-56.)
Saturated Fat Slows Blood Flow in the Arteries
Here is what recent studies found about how saturated fat essentially clogs the arteries. (The endothelium is the layer of cells lining the inside of blood vessels and arteries. It is important in regulating blood flow.)
“High SFA (saturated fat) caused deterioration in FMD (flow-mediated dilation) compared with high PUFA, MUFA, or CARB diets. Inflammatory responses may also be increased on this diet.” (Arterioscler Thromb Vasc Biol. 2005 Jun;25(6):1274-9.)
And:
”Consumption of saturated fat reduces the anti-inflammatory potential of HDL and impairs arterial endothelial function. In contrast, the anti-inflammatory activity of HDL improves after consumption of polyunsaturated fat.” (J Am Coll Cardiol. 2006 Aug 15;48(4):715-20.)
And:
“Consumption of an SAFA-rich meal is harmful for the endothelium, while a MUFA-rich meal does not impair endothelial function in subjects with type 2 diabetes.” (Diabetes Care. 2008 Dec;31(12):2276-8.)
Overall, you should be able to see that the case against too much saturated fat in the diet is convincing – one way or another — and it’s not just about cholesterol. Bear in mind that vegetable sources of saturated fat are not inconsequential. Olive and soy oil are about 15%, corn and sunflower about 12% and peanut oil around 20%. However, consuming saturated fat and cholesterol together in animal foods may present the greatest combined risk, and whole nuts or seeds, even with some saturated fat, the least risk.
- Parrott MD, Greenwood CE. Dietary influences on cognitive function with aging: from high-fat diets to
healthful eating. Ann N Y Acad Sci. 2007 Oct;1114:389-97. Review.
- Laitinen MH, Ngandu T, Rovio S, et al. Fat intake at midlife and risk of dementia and Alzheimer’s disease: a
population-based study. Dement Geriatr Cogn Disord. 2006;22(1):99-107.
- Morris MC, Evans DA, Bienias JL, et al. Dietary fats and the risk of incident Alzheimer disease. Arch Neurol. 2003 Feb;60(2):194-200. Erratum in: Arch Neurol. 2003
- Vessby B, Unsitupa M, Hermansen K, et al. Substituting dietary saturated for monounsaturated fat impairs insulin sensitivity in healthy men and women: The KANWU Study. Diabetologia. 2001 Mar;44(3):312-9.
- Riccardi G, Giacco R, Rivellese AA. Dietary fat, insulin sensitivity and the metabolic syndrome. Clin Nutr. 2004 Aug;23(4):447-56. Review.
- Keogh JB, Grieger JA, Noakes M, Clifton PM. Flow-mediated dilatation is impaired by a high-saturated fat diet but not by a high-carbohydrate diet. Arterioscler Thromb Vasc Biol. 2005 Jun;25(6):1274-9.
- Tentolouris N, Arapostathi C, Perrea D, et al. Differential effects of two isoenergetic meals rich in saturated or monounsaturated fat on endothelial function in subjects with type 2 diabetes. Diabetes Care. 2008 Dec;31(12):2276-8.
- Nicholls SJ, Lundman P, Harmer JA, et al. Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function.J Am Coll Cardiol. 2006 Aug 15;48(4):715-20.
Dioxins in Food and Water Could Cause Diabetes
By Paul Rogers
Agent Orange - from imjoshdotcom
I’ve been aware of an increasing number of recent studies that seem to show that the chemical pollutants called POPs – dioxins and similar compounds – could be at least partly responsible for the current epidemic of type 2 diabetes. Now it’s not conclusive, but some aspects of these investigations are certainly interesting. Like the fact that when controlled for dioxin content of tissue, even obese people were at no higher risk of type 2 diabetes if their dioxin levels were low. This could be a chance occurrence, or other factors could cause this to occur, but overall there are some compelling aspects to this research.
Here is what one author had to say:
“The strong associations seen in quite different studies suggest the possibility that exposure to POPs could cause diabetes. One striking observation is that obese persons that do not have elevated POPs are not at elevated risk of diabetes, suggesting that the POPs rather than the obesity per se is responsible for the association. ” [Rev Environ Health. 2008 Jan-Mar;23(1):59-74. Review.]
POPs are “persistent organic pollutants.” This class of pollutants includes dioxins, PCBs, DDT, DDE and many chlorinated organic pesticides. They accumulate in your body and in the fat of the animals we eat.
History of Dioxins and Diabetes
Some years ago I worked in occupational and environmental health and safety, advising on toxic chemicals and health. As well as working to establish the first chemical list for Australia’s National Pollutant Inventory, I also helped out the local Vietnam vets with their Agent Orange herbicide case. Much of the finer detail of the toxic risk assessments involved dioxins — exotic chemical contaminants that result from chemical manufacture and combustion. Levels of dioxin were very high in Agent Orange. There are over 200 varieties of dioxins, furans and polychlorinated biphenyls (PCBs) – chemicals with somewhat similar structure and varying toxicities to humans. Sometimes the toxicity of these dioxin-like chemicals are referred to collectively with ‘toxic equivalents’ or TEQ.
Studies of manufacturing workers exposed to dioxins and similar compounds had already revealed a higher incidence of diabetes, and animal tests had confirmed this possibility to some degree.
The early emphasis of dioxin toxicity research was on birth defects and cancer. However, it took some time for the US Veterans Affairs Department to acknowledge limited evidence in support of a connection of Agent Orange exposure with type 2 diabetes, to the extent that disability pensions are now paid on this basis.
Other pieces of research seem to fit the puzzle. It seems that endocrine disrupting chemicals in general, especially ones that persist in the environment, are associated with diabetes. And a most recent research study suggests that the much-publicized plastics residue bisphenol-A is also possibly involved.
POPs and Diabetes: What You Can Do
While these contaminants are everywhere – from the Antarctic to the purest looking lake water – they also contaminate food by accumulating in animal fats – and which we consume in meat, chicken, dairy and fish products and fats.
If you want to reduce your intake, you really need to either find wild or organic and lean products from pristine places, or reduce your intake of animal foods, especially fat, or perhaps do a combination of both. This issue is also another reason why high-meat and fat diets like Atkins low-carb can be a recipe for disaster. And as for those so-called diet gurus who say we should eat more saturated fat . . . here’s a very good reason not to.
- Rignell-Hydbom A, Rylander L, Hagmar L. Exposure to persistent organochlorine pollutants and type 2 diabetes mellitus. Hum Exp Toxicol. 2007 May;26(5):447-52.
- Rylander L, Rignell-Hydbom A, Hagmar L. A cross-sectional study of the association between persistent organochlorine pollutants and diabetes. Environ Health. 2005 Nov 29;4:28.
- Ropero AB, Alonso-Magdalena P, García-García E, Ripoll C, Fuentes E, Nadal A. Bisphenol-A disruption of the endocrine pancreas and blood glucose homeostasis. Int J Androl. 2008 Apr;31(2):194-200. Epub 2007 Oct 31. Review.
- Wang SL, Tsai PC, Yang CY, Leon Guo Y. Increased risk of diabetes and polychlorinated biphenyls and dioxins: a 24-year follow-up study of the Yucheng cohort. Diabetes Care. 2008 Aug;31(8):1574-9. 2008 May 16.
- Michalek JE, Pavuk M. Diabetes and cancer in veterans of Operation Ranch Hand after adjustment for calendar period, days of spraying, and time spent in Southeast Asia. J Occup Environ Med. 2008 Mar;50(3):330-40.
Recommended Dietary Intakes - Do You Need Supplements?
By Paul Rogers
Photo by Untitled Blue
Here’s a quick definition of RDIs — or RDAs as they are called in some countries.
Optimising Diets for Chronic Disease Risk
Other Standards in Nutrient Reference Values
- EAR (Estimated Average Requirement). A daily nutrient level estimated to meet the requirements of half the healthy individuals in a particular life stage and gender group.
- RDI (Recommended Dietary Intake). The average daily dietary intake level that is sufficient to meet the nutrient requirements of nearly all (97–98 per cent) healthy individuals in a particular life stage and gender group.
- AI (Adequate Intake - used when a recommended dietary intake cannot be determined). The average daily nutrient intake level based on observed or experimentally-determined approximations or estimates of nutrient intake by a group (or groups) of apparently healthy people that are assumed to be adequate.
- EER (Estimated Energy Requirement). The average dietary energy intake that is predicted to maintain energy balance in a healthy adult of defined age, gender, weight, height and level of physical activity, consistent with good health. In children and pregnant and lactating women, the EER is taken to include the needs associated with the deposition of tissues or the secretion of milk at rates consistent with good health.
- UL (Upper Level of Intake). The highest average daily nutrient intake level likely to pose no adverse health effects to almost all individuals in the general population. As intake increases above the UL, the potential risk of adverse effects increases.
- AMDR (Acceptable Macronutrient Distribution Range). An estimate of the range of intake for each macronutrient for individuals (expressed as per cent contribution to energy), which would allow for an adequate intake of all the other nutrients whilst maximising general health outcomes.
- SDT (Suggested Dietary Target). A daily average intake from food and beverages for certain nutrients that that may help to prevent chronic disease.
Dietary Supplements
Supplementation has a role to play, but it needs to be done with caution, restraint and knowledge. The bottom line is that there will be individuals and population groups that do not meet the RDIs for individual nutrients.
- This can result from poor nutrition practices or even special diets poorly implemented. Low-carbers could be short on fibre and vitamin E; vegans on zinc, iron and B12; and very low-fat dieters on long chain omega-3.
- Populations in nutrient poor regions might lack iodine and selenium; and certain cultural habits like full body clothing can result in inadequate vitamin D intake in the absence of food or supplement sources.
- Athletes and heavy exercisers may need a modest increase in some nutrients, but this is usually accounted for by increased calorie intake — as long as the extra food is nutrient dense for the most part.
- Older people absorb vitamin B12 less well and this may require supplementation. The ill or infirm who do not get adequate sun exposure may require vitamin D supplements.
- Pre- and during pregnancy, folate supplementation is a useful reassurance against neural tube abnormalities.
However, not only is it likely wasteful to take mega-doses of supplements, it may even be unsafe. The recent scientific examination of vitamin E and beta carotene in high supplement doses has not yielded promise and has suggested adverse effects. If you feel you need to take an individual supplement or a multi, first check out the excellent information at the Office of Dietary Supplements at the NIH. then try not to exceed the RDI by more than a few times for any individual nutrient, unless there are indications that it’s safe and effective to do so.
Food and Fitness Science Roundup
By Paul RogersFor this regular roundup, I try to find work that tells us something significant or new in the context of the field of study.
New Recommendations for Vitamin D Intake for Children from the American Academy of Pediatrics
A recommendation for a doubling of recommended dietary intake of an essential nutrient for any population sector is substantial news in nutrition science. The AAP list the reasons and the strategy here.
http://www.aap.org/pressroom/nce/nce08vitamind.htm
Coffee Drinking Does not Raise Mortality
Up to 6 cups a day and risks were still normal and even slightly lower than the consumers of much more moderate quantities. Adjustment of cardiovascular risk seems to be the difference — perhaps by lowering the risk of type 2 diabetes?
Ann Intern Med. 2008 Jun 17;148(12):904-14. The relationship of coffee consumption with mortality. Lopez-Garcia E, van Dam RM, Li TY, Rodriguez-Artalejo F, Hu FB.
Also see: Does Coffee Kill or Cure?
Red Wine Seems to Cut Risk of Lung Cancer
What? Not another reason to drink red wine! The authors do counsel against excessive consumption.
Cancer Epidemiol Biomarkers Prev. 2008 Oct;17(10):2692-9. Alcoholic Beverage Intake and Risk of Lung Cancer: The California Men’s Health Study. Chao C, Slezak JM, Caan BJ, Quinn VP.
Vitamin C Interferes with Training Adaptation and Performance
I noticed the possibility of this a few years ago while researching the utility of antioxidants like vitamin C to benefit athletic performance. Vitamin C seemed to inhibit phosphofructokinase, which is an important enzyme in glycolysis (breakdown and use of glucose for energy). Considering that many athletes and fitness buffs seem to take vitamin C supplements, it may be worth noting. Moderate dietary intake is likely not a problem. We need more information on this one before the panic sets in.
Am J Clin Nutr. 2008 Jan;87(1):142-9. Oral administration of vitamin C decreases muscle mitochondrial biogenesis and hampers training-induced adaptations in endurance performance. Gomez-Cabrera MC, Domenech E, Romagnoli M, Arduini A, Borras C, Pallardo FV, Sastre J, Viña J.
Caffeine Plus Carbohydrate Increases Glycogen Storage
As far as I am aware, this is the first time this has been shown. About 500 mg caffeine is a lot of coffee though.
J Appl Physiol. 2008 Jul;105(1):7-13. High rates of muscle glycogen resynthesis after exhaustive exercise when carbohydrate is coingested with caffeine. Pedersen DJ, Lessard SJ, Coffey VG, Churchley EG, Wootton AM, Ng T, Watt MJ, Hawley JA.
New Glycemic Index and Load Tables
If you’re into the GI, you’ll need this. More on the GI in another article. I’m not a big fan.
Click through to here from the abstract and you can download the free tables.
Diabetes Care. 2008 Oct 3. International tables of glycemic index and glycemic load values: 2008. Atkinson FS, Foster-Powell K, Brand-Miller JC.
Check out the Food for Life, Fit for Life Training Program. Free download available.
Food for Life, Fit for Life - Lifestyle Training Course Released
Food for Life, Fit for Life - Prevent Diabetes, Heart Disease and Cancer is a set of training modules in lifestyle preventive health. It took me 12 months to write and it’s now available for licensing. You can download a free ebook version that describes the content. Here’s what’s included:
- Training and evaluation manual for course presenters
- 120 PowerPoint slides with notes and contemporary references
- Sample learner assessment questions for each module
- Fact sheets that can be used as handouts to clients/students
- Risk evaluation self-assessment handouts for nutrition, physical activity, diabetes, cardiovascular disease, and cancer
- Case studies for workgroups and workshops
- Glossary of terms
- Regular newsletter
- US and UK/Australia versions (spelling and units)
- Evidence based information, fully referenced
- Flexible licence conditions and regular, free updates for one year
- Access to a membership web site for support, updates and extra resources.
Background
I started writing this over 12 months ago as a tool to use for talks to clients and groups in fitness and personal training. Rather than the limited training course I had in mind at that time, it has now morphed into something more like a training ‘environment’ with support tools like handout risk assessments and case study tasks. I have plans to add more of these tools and content within the context of the course. For example, a basic ’sports nutrition’ module is near completion.
As a trainer-presenter, your options are varied. You could select various slides or modules for presentations ranging from 2 hours to 2 days to groups or even individual clients. The target audience could include lay people or professionals in various support roles in preventive health. Presenters could include dietitians, nutritionists, fitness trainers, practice nurses, physios, diabetes educators and any support professionals working in preventive and lifestyle health. Some skill in delivering an appropriate language and idiom to audiences with variable knowledge bases would be required by the presenter.
I’ve summarised the essential elements of lifestyle disease, meaning the risks with which we burden ourselves because of our behaviour in relation to food, nutrition and physical activity. Although I mention the roles of environment and genetics, this is not the focus of the program at this time, but I do have plans to add modules that address basic issues in environmental safety in relation to food quality. Any additional modules added are included in the updates available in the licence for one year.
The core elements are:
- Type 2 Diabetes
- Cardiovascular disease
- Cancer
- Obesity
- Motivational and behavioural change
- Nutrition
- Physical activity and exercise
For example, I’ve summarised the complete content of the WCRF/AICR Expert Report: Food, Nutrition, Physical Activity and the Prevention of Cancer: a Global Perspective so that the essential points are clear.
Licences
At present, only one licence option is available. This locks the headers and footers and PowerPoint attributions to me and no changes are permissible. I will probably also offer a ‘professional licence’ under which the licensee has the right to modify the content and replace attribution and headers etc with their identity. This would allow the licensee, with some restrictions, to modify the content and to adjust any particular aspect that did not suit their purpose or premise.
Availability
I’ve created a free ebook (pdf) version of the course, featuring the PowerPoint slide headings with content from the notes of each slide. This delivers a summary version and illustrates the content quite successfully. Not everything is fleshed out of course.
The best way to get this is to fill out the email form on the front page of the web site — or on this blog at the top right. This will redirect to a download page after confirmation. You will then get an email advising when content is updated or added, including new web and blog articles. This would be no more frequent than once each week.
I hope you take a look at the free ebook and let me know what you think. Suggestions, comments and admonitions are, of course, welcome.
Low-Carb Diets Make You Dumber and Slower
By Paul Rogers
Photo courtesy Anosmia
Low-carb diets have had their share of weight loss success; and most of it can be attributed to dietary restriction of food choice. That’s how most restrictive diets work, from low-fat to low-carb and vegan: tell people they can’t eat something that’s clearly identifiable, and they will lose weight because choice is curtailed and they find it easier to eat fewer calories.
The trouble starts when they find they can’t maintain such a restrictive regimen — and then they get discouraged, guilty, and the relapse occurs.
But what if low-carb dieting helped you lose weight for the time being, but actually inhibited your personal performance in day-to-day living? Would you continue with it as a lifestyle choice?
What I’m about to discuss does not necessarily apply to moderately low-carb diets, but mostly to ketogenic diets, in which carbohydrate intake is usually less than 20 percent. Even so, there is a possibility that the effects apply across a continuum of low-carb eating from very low to low.
And those adverse effects? Low-carb makes you think slower and move slower.
Low Carb Makes You Dumber
In a study in 2007 in the American Journal of Clinical Nutrition, researchers compared the cognitive abilities of dieters on a low-carb, high-fat (LCHF) diet with another group of dieters on a high-carb, low-fat diet (HCLF) . Here is what they found:
However, the IT test score (a measure of the speed of visual information processing) was affected by diet composition. The results showed that participants consuming the LCHF had significantly less improvement in the minimum stimulus time required to make a correct response than did those consuming the HCLF diet . . . Our findings are consistent with those of an earlier study in obese women showing that performance of a complex, cognitively demanding task assessing mental flexibility was significantly worse after the consumption of a very-low-energy, low-carbohydrate, ketogenic diet than after the consumption of an isocaloric, nonketogenic diet with higher carbohydrate and lower fat content. Similarly, the treatment of young rats with a ketogenic LCHF diet for 1 month resulted in severe cognitive impairment, and a series of rat studies showed that the chronic ingestion of a high-fat diet, in particular a high-saturated-fat diet, can adversely affect cognitive performance.
Low Carb Makes You Slower
In a study in the Journal of the American Dietetic Association in 2007, a team of investigators measured the fatigue and perceived effort of one group of dieters on a ketogenic low-carb diet and another group on a diet with much higher quantities of carbohydrate. Here’s what they concluded:
These pilot data indicate that ketogenic, low-carbohydrate diets enhance fatigability and can reduce the desire to exercise in free-living individuals.
This is not surprising because athletes know that glucose (and phosphocreatine) supply energy at a rate that supports fast, high-powered activities, whereas fat and ketones can only supply energy at a rate biochemically rapid enough for mostly slower activities.
Evidence from the Paleolithic
Now, you might think that would be a good place to leave this discussion — the evidence is reasonably clear — but just for speculative fun, let’s take a look at our evolutionary pre-history and the diets of emerging Homo sapiens — modern humans — in the Paleolithic period of evolution.
About 800,000 years ago, primates moved out of Africa to the north and into Europe to colder climates. This early pre-human form was called Homo erectus, and this species probably evolved into Homo neanderthalis, the Neanderthals, while erectus lived on as a parallel species.
The curious thing is that a second migration of early humans north from Africa started about 50,000 years ago and spread throughout Europe and beyond. It seems that this smart new species, Homo sapiens or ‘intelligent human’, was much more intelligent than earlier species such as erectus and neanderthalis. As far as evolutionary science can establish, Homo sapiens swept all before it and replaced the Neanderthals and erectus with modern humans throughout the world. The other species were out-competed and did not survive.
Paleo Diets and the Evolution of Power and Intelligence
Enthusiasts of Paleo dieting like to contend that early humans were very healthy on a diet mostly of meat, vegetables and some fruit, but virtually no grains or tubers — that is, a low-carbohydrate diet. However, it’s pretty clear that early humans started to eat grains about 20,000 years ago, perhaps earlier, and, according to Richard Wrangham, Elizabeth Pennisi and others, probably ate tubers well before then. See Did Cooked Tubers Spur the Evolution of Big Brains?
Paleontologists have speculated as to why Homo sapiens so dominated the other species in Europe and beyond as they moved into their territory from 50,000 years ago.
Here’s where I speculate that the burgeoning consumption of carbohydrate foods in the form of tubers and grains in East Africa, the cradle of early humans, fed a growing brain that thrives on glucose. Glucose from carbohydrates supplied abundant energy substrate for the evolving brain to build those complex neural networks that we know provides the complex reasoning capabilities of modern humans.
Carbohydrate foods were abundant in the East African savannah. As Wrangham points out: “Today, there are 40,000 kilograms of tubers per square kilometer in Tanzania’s savanna woodlands.” The book The Lost Crops of Africa, documents the prolific grain resources in this region. It would be unlikely if the evolving Homo sapiens did not take advantage of these abundant food resources at some time.
The Neanderthals, by comparison, most likely had a more limited food supply, relying mostly on meat and some vegetables and fruits in season, and eggs but fewer carbohydrate resources, especially in the cold north.
I think it’s a fair bet that Homo sapiens, as they moved north out of Africa from 50,000 years ago, armed with complex brains fueled by rapidly accessible glucose from carbohydrate food resources, simply out-competed the slower moving and thinking Neanderthals and the remaining Homo erectus. Not only were modern humans smarter, they probably moved faster as well.
The thing is, we can still simulate the best qualities of the diets of our ancestors, which were most likely characterised by being low in saturated fat, high in plant foods and fibre, and with sufficient carbohydrate to keep us out of ketosis and to fuel the powerful movement and activity required for good health and fitness.
High carb. Simply smarter, faster.
American Journal of Clinical Nutrition, Vol. 86, No. 3, 580-587, 2007
J Am Diet Assoc. 2007 Oct;107(10):1792-6.
Exercise Really is Necessary to Maintain Weight
By Paul Rogers
Pic from mikebaird
Recently I got into a discussion about whether exercise is really necessary in a weight loss program. The other guy was saying . . . ‘well, if you just cut calorie intake you’re going to lose weight . . . if you starve you lose weight; witness concentration camps and so on’. And of course, Gary Taubes has been stirring up the diet and exercise community with his irreverent, but flawed views.
It’s a trite argument isn’t it? If you don’t eat, or eat very little, inevitably you will lose weight, fat and muscle. We all know that; except that’s not what we’re really talking about today. If you’re overweight you need to find a pattern of living that allows you to maintain a normal weight and eat well enough so that you enjoy life without having to do “diets”.
What I recommend is moderate calorie restriction in conjunction with a substantial increase in physical activity. And I’m not alone. Increasingly the science supports this, as do many successful weight losers.
Calorie-restricted diets
The trouble with low-calorie diets by themselves is threefold:
- You reset your metabolism — downward. This is diet-induced thermogenesis. The body senses a low-calorie environment and decides to reduce its basal energy expenditure. It’s a survival mechanism that’s evolved over thousands of years.
- On low-calorie diets you lose not only muscle, but bone as well. Okay, when you stabilise your weight you may get some of this back, but it’s not ideal.
- Without exercise, you don’t get all those other proven benefits like protection from heart disease and some cancers, improved bone density, mental health, and perhaps protection from dementias as well as a list of other benefits.
Proven as a practical approach
Professional physical activity guidelines have for several years recommended that one needs to exercise an hour a day for most days of the week to lose weight and to keep it off. This has recently been confirmed by a study of women published in the Archives of Internal Medicine
Not only that, but the US National Weight Control Registry – a program that keeps track of successful weight losers — found that most of their successful listers did just that: exercised for about an hour a day in addition to their day-to-day activities. It doesn’t have to be all high-intensity stuff, because many did a lot of walking.
Low energy density, high-nutrient foods
One way to trick the body into maintaining metabolism while you reduce calorie intake is to eat plenty of low energy density foods — along with the increase in exercise. That means fruit and vegetables, salads, soups, bowl foods, beans, lean meat and not too much fat, refined carbohydrates and sugars. This is a proven approach called Volumetrics, which originated with Barbara Rolls at Pennsylvania State University.
Giving the body plenty of fibre, water and bulk to deal with even though the calorie count is comparatively low, tends to keep that metabolism from dropping too much.
Exercise - the fourth macronutrient
Food pyramids increasingly include physical activity in their recommendations because the best evidence suggests that uncoupling physical activity from food consumption creates a body environment that is not ideal for weight loss and maintenance, or health. This also reflects an evolutionary state built over tens of thousands of years when early humans moved much more than we do today.
I understand that some people can’t do much exercise. The infirm, injured and invalid have additional challenges, but the effort may be just as important for many people in this situation.
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