Sometimes it seems difficult to understand how our food choices could have such a significant effect on our health. Many people believe that as long as they provide their body with energy and protein along with some sources of nutrients that they are good to go. It must be pointed out that the human body is an astonishingly complicated mechanism requiring a vast number of biochemical reactions and interactions with requirements for numerous ingredients such as enzymes, co-factors, vitamins, minerals and trace elements just to keep a person alive. It is estimated that the number of reactions within ONE single human cell numbers in the hundreds of millions to several billion PER SECOND. With this in mind it is not hard to imagine that a lack of proper nutrients can disrupt some of these functions. We know that human beings can survive on a wide range of foods but, if you’re striving for the best chance of gaining tip-top health, it seems appropriate to consume foods that offer the highest concentration of the nutrients that the body needs to thrive.
There is much discussion in nutrition today about the abundance of health benefits derived from eating whole foods compared to the profusion of health-damaging effects resulting from the consumption of processed foods. Why is it better for your body to eat a food that is relatively unchanged from the way it is found in nature? The crux of this matter is that our bodies treat whole foods in a vastly different manner than they treat processed foods. Let’s dig into some of the processes in the human body that metabolize and absorb nutrients to discover how your body actually deals with the food you consume.
METABLISM AND ABSORPTION OF ISOLATED MACRONUTRIENTS SUCH AS THOSE FOUND IN PROCESSED FOODS
Macronutrients include carbohydrates, proteins and fats but the two that we are interested in here are fats and carbohydrates. The following is a summary of what happens when these ingredients are received in the stomach as isolated or added ingredients such as when consuming vegetable oils, processed foods, refined sugars or refined carbohydrates.
Added Fats (1,2)
Isolated fats are digested and absorbed both in the stomach and the small intestine. Fat digestion begins in the mouth through the action of the enzyme lingual lipase and continues in the stomach with the help of another enzyme, gastric lipase, and then in the small intestine with pancreatic lipase. Fats are hydrophobic, meaning that they will not dissolve in water-based environments such as that of the stomach, leaving digestive enzymes with only the outer surface of fat globules to work on. Smaller fat globules allow the digestive process to proceed much more quickly and muscular action in the walls of the small intestine (peristalsis) does a fairly good job of breaking down fat globules into smaller particles. These fat droplets are then coated with bile salts to prevent them from re-associating with each other (emulsification) and turning back into larger particles. Colipase, a protein assistant to the enzymes, binds to the surface of the fat droplets and helps to anchor lipase enzymes to them so that digestion, the breaking down of fat droplets to release their basic components, can occur.
Lipids derived from the diet are 90% triglycerides and the balance consists of phospholipids and cholesterol. After the breakdown of the fat droplets, basic lipids such as fatty acids, monoglycerides and cholesterol are liberated and they quickly associate with bile salts to form micelles. Micelles are about 200 times smaller than fat droplets. They transport fats to the surface of the enterocyte cells, the specialized epithelial cells that line the small intestine. Micelles are small enough to fall between the microvilli, tiny projections on the surface of enterocytes that increase the surface area of the intestine to allow more absorption of nutrients. At this point the micelles can break down into their basic fat components that can simply diffuse across the enterocyte membrane although specific transport proteins are also available to aid their passage into the cells. Once inside the enterocyte the fat molecules are repackaged, along with fat-soluble vitamins, into chylomicrons, special particles that are designed for the transport of lipids in the bloodstream. The chylomicrons are then re-released into the small intestine. Chylomicrons are generally too large to enter tiny blood capillaries. Instead they enter the lymph vessels that are located in the center of each enterocyte. These vessels drain into the general circulation at the large veins in the chest which then carry the chylomicrons to the cells of the body. There they are opened by lipoprotein lipase, an enzyme found in the walls of the endothelial cells lining the walls of blood vessels, and their lipid contents are released from the chylomicrons to diffuse into cells.
Added refined sugars and refined carbohydrates (3,4,5,6)
Simple carbohydrate sugars include monosaccharides (glucose, fructose and galactose) and disaccharides (maltose, lactose and sucrose). Disaccharides must be broken down, with the help of their own specific enzymes, into monosaccharides in order to be absorbed. For example, the enzyme maltase cleaves maltose into two molecules of glucose. The enzyme lactase cleaves lactose into a glucose and a galactose molecule and the enzyme sucrase cleaves sucrose into a glucose and a fructose molecule. These sugar-digesting enzymes are found in the small intestine, tethered to the enterocyte cells that line the intestines. Specific transporter proteins then carry the monosaccharides into the enterocytes and across the cell membrane into the bloodstream. This process is straightforward and leads to a sharp rise in both blood sugar levels and insulin release by the pancreas within about 15 to 20 minutes.
Results of the consumption of added refined carbohydrates and isolated fats
Highly processed and calorie-dense foods lead to exaggerated after meal spikes in blood sugar and fat which in turn generate immediate oxidative stress that increases in direct proportion to the magnitude of the upsurge of blood glucose and triglyceride (fat) levels after a meal. Production of free radicals ensues which triggers changes in the cardiovascular system including inflammation, thickening of the blood and reductions in artery function. These effects occur within one or two hours after eating. Just as continuous blows of a hammer on a finger can only produce an increasingly mutilated digit with no possibility of healing, unceasing assault to the body through eating unhealthy foods meal after meal sets up conditions that encourage the development of heart disease, diabetes, obesity and other chronic afflictions now suffered by our modern society. In fact this after-meal “dysmetabolism” is an independent predictor of future cardiovascular events in both diabetes and non-diabetics. (7)
METABOLISM AND ABSORPTION OF MACRONUTRIENTS FROM WHOLE PLANT FOODS
Studies on the consumption of minimally processed, high fiber, whole plant foods illustrate time and time again a marked decrease in after-meal upsurges of blood sugar and fat levels and inflammation, preventing the inflammatory cascade described above that leads to ill health (7). The digestion of whole foods is markedly altered from the basic process that occurs with isolated or added fats. Firstly, breakdown of a whole food is delayed by its physical structure. Its sugars and fat are an integral part of its fibrous physical matrix and are released later in the process and much more slowly. More significant however are other factors inherent in whole foods which transform the whole digestion process. The following is an overview of what is known so far about how whole foods promote a significantly healthier metabolism.
Phytochemicals are chemical compounds produced by plants that have biological activity in the plant itself, helping them to not only thrive but to thwart competitors, predators, or pathogens. Phytochemicals in fruits and vegetables have been shown to reduce dysmetabolism in humans. The benefits they offer stem from their antioxidant, anti-inflammatory, and anti-clotting properties. Phytochemicals reduce the production of free radicals (reactive oxygen species (ROS)) that is the usual result of inflammation and they also scavenge ROS that do form, thereby inhibiting cellular damage at many levels. In addition they antagonize the function of the major molecules involved in inflammation (nuclear factor-KB, tumour necrosis factor-alpha, interleukin-6, inducible nitric oxide synthase activity and monocyte chemotactic protein-1). Moreover phytochemicals have the ability to prevent platelet-induced blood clotting activity and to enhance nitric oxide production in the endothelium. (17) (For more information on the endothelium, see the blog entitled “What Does Eating Plants Do For Your Blood Vessels?”)
Phytochemicals also have the ability to stimulate the immune system, prevent toxic substances in the diet from becoming carcinogenic, slow the growth rate of cancer cells, reduce inflammation and oxidative damage to cells, trigger damaged cells to self-destruct before they can reproduce, prevent DNA damage, aid DNA repair and regulate hormone signalling and gene expression (9). Interestingly, present research is revealing that antioxidant activity is significantly reduced during metabolism and it appears that antioxidant effects on cell signaling and gene expression may be more important for good health than direct antioxidant activity. Even low levels of phytochemicals in blood and tissues display these indirect effects (10,11).
Growing evidence indicates that foods rich in polyphenols, a sub-type of antioxidants, are particularly effective at reducing after-meal blood sugar levels and improving insulin secretion and insulin sensitivity. They do this by inhibiting carbohydrate digestion and glucose absorption in the intestine, modulating glucose release from the liver, stimulating insulin secretion from the pancreas, activating insulin receptors which allow glucose intake into blood cells and by modulating gene expression. Through these actions polyphenols in whole foods can prevent insulin resistance, metabolic syndrome and type-2 diabetes (9,31).
Polyphenols are also capable of altering the ratio of bacterial types in the gut microbiome towards promotion of healthy BMIs. Polyphenols increase levels of Bacteroidetes and Actinobacteria which are prominent in lean people while discouraging Firmicutes and Proteobacteria, the more prevalent bacterial species in the microbiomes of obese people. This action has the effect of decreasing obesity thereby significantly reducing risk factors for many chronic diseases (13).
Other clinical effects of antioxidants include the following;
Lowering of blood pressure (19,20,33)
Promotion of relaxation of blood vessels (26,27,28)
Inhibition of very early stages of atherosclerosis (21)
Protection of cardiac tissue from cell death (23)
Prevention of heart dysfunction (24)
Inhibition of inflammation and platelet activation (18)
Suppression of the formation of new fat cells and stimulation of fat breakdown (8,22)
Lowering of LDL levels (25,32,34,35,36)
Decreasing total cholesterol, LDL, triglycerides, and ApoB levels in patients with diabetes and cardiovascular risk factors (29,30)
Whole foods such as fruits, vegetables, legumes, whole grains, nuts and seeds are excellent sources of fiber while processed foods contain little if any. Animal products such as dairy and meat contain no fiber at all. High-fiber foods are metabolized quite differently than low-fiber foods.
Fiber in whole foods decreases the amount of energy from that food that can be metabolized and absorbed. This is because the digestibility of fat from a food decreases as its dietary fiber increases. Also, as dietary fiber increases, the intake of simple carbohydrates tends to decrease. Dietary fiber itself contributes to the total calories derived from a food but fiber is resistant to digestion by the small intestine and even presents a digestion challenge in the large intestine. In fact, in spite of fiber being a member of the carbohydrate family, it provides fewer calories per gram than the 4 calories per gram of most carbohydrates. Fiber fermented by bacteria (about 70% of total fiber) actually provides about 2 calories per gram, and insoluble fibers, which defy digestion and are eliminated mostly intact, do not contribute any calories at all (12,41).
Studies have found that adequate fiber intake consistently lowers the risk of cardiovascular disease and coronary heart disease through reduction of LDL (low density lipoprotein), reduction of C-reactive protein (a measure of inflammation) and reduction of blood pressure (37,39). Studies also show that the more fiber consumed, the lower the risk of diabetes (37). Fiber provides a high degree of meal satisfaction through the increased time required to chew fiber-rich foods and the feeling of satiety from greater stomach fullness. Fiber also slows stomach emptying time, decreases the rate of glucose absorption in the small intestine and reduces insulin response. Prospective cohort studies report that those consuming more fiber weigh less than those who consume less fiber. One study reported that every 1 gm increase in the total amount of fiber consumed daily decreased body weight by 0.25 kg (39,40).
Some types of fiber act as prebiotics, non-digestible food ingredients that selectively stimulate the growth and/or activity of “good” bacteria in the colon resulting in improved host health. This generally refers to the fiber’s effect on bifidobacteria and lactobacilli, both of which are beneficial to human health. Benefits include improved gut barrier function and immunity, increased production of SCFAs (short chain fatty acids – see more information in the next section) and reduction of potentially pathogenic bacteria such as clostridia (37).
Microflora of the large intestine
Depending on the source referred to, the number of bacteria living in and on the human body outnumber human cells by a factor of anywhere from 1.3: 1 to 10:1 (38). The vast majority of this microflora resides in the large intestine. It is not surprising that this huge symbiotic population of bacteria exerts an enormous influence on human health. Eating whole foods delivers fiber to the large intestine, the magic component for a robust and health-giving intestinal microflora.
The food we eat is our main contact between our inner organs and the outer world. Epithelial cells make up many parts of our body. They form the outer portion of our skin, line the outer surfaces of organs and blood vessels throughout the body and also the inner surfaces of cavities in many internal organs. It is a specialized type of epithelium that lines our intestines where it is only a single cell deep, a microscopic barrier between two vastly different environments. Our gut bacteria are a major component of the protective force of our immune system, our “body guard” against potential hazards from our surroundings.
Gut microbes are capable of producing a vast range of products. However, the most abundant and important ones are the short chain fatty acids (SCFAs), acetate, propionate and especially butyrate. Butyrate is the preferred energy source for the epithelial cells of the colon (the large intestine) and the beneficial bacteria present in the colon rely on fiber from which to produce this molecule (14). Butyrate plays an important role in the maintenance of health and the prevention of disease through its interactions with receptors in the large intestine. An astounding variety of advantageous effects result from these interactions including the regulation of immune function (SCFAs increase the numbers of T-helper cells, macrophages and neutrophils and the activity of natural killer cells), inflammation, metabolism and disease. There is emerging evidence of increased resistance to illness and infection with higher fiber intake. Ongoing research continues to strengthen the link between diets high in fiber that feed our “good” bacteria and the reduced risk of chronic diseases such as heart disease, diabetes and obesity (15,16,37) as well as lower mortality from circulatory, digestive and inflammatory diseases (37).
TO SUM IT ALL UP….
It is clear that our food choices matter immensely for our health. Though this might seem to lay a huge burden on us in our daily lives, in reality it does not. In spite of the extreme complexity of the bodily processes necessary for life, our path is simple. There is no need to calculate how much of this nutrient or that food we should be consuming. We can simply eat generous amounts of a wide variety of whole plant foods including fruits, vegetables, whole grains, legumes, nuts and seeds and our bodies will have all the raw materials it needs to keep us in the best health possible.
2 Bauer, E., Jakob, S., Mosenthin, R. Principles of Physiology of Lipid Digestion. Institute of Animal Nutrition, University of Hohenheim, Stuttgart, Germany August 12, 2004; 282-295.
3 Jenkins, D.J.A., Jenkins, A.L., Wolever, T.M.S., Thompson, L.H., Rao, A.V. Simple and Complex Carbohydrates. Nutrition Reviews February 1986; 44(2): 42-49.
6 Miller, R., Stanner, S. A summary of evidence on the digestion, absorption and metabolism of white
bread carbohydrates. British Nutrition Foundation. 2016.
7 J O’Keefe, J.H., Gheewala, N.M., O’Keefe, J.O. Dietary strategies for improving post-prandial glucose, lipids, inflammation, and cardiovascular health. Am Coll Cardiol. 2008 Jan 22; 51(3): 249-255.
8 Meydani, M., Hasan, S.T. Dietary polyphenols and obesity. Nutrients. 2010 Juyl ;2(7): 737-751
9 Hanhineva, K., Törrönen, R., Bondia-Pons, I., Pekkinen, J., Kolehmainen, M., Mykanen, H., Poutenen, K. Impact of Dietary Polyphenols on Carbohydrate Metabolism. Int. J. Mol. Sci. 2010; 11(4): 1365-1402.
10 Gordon, M.H. Significance of dietary antioxidants for health. Int J Mol Sci. 2012; 13(1): 173-179.
11 Tsao, R. Chemistry and biochemistry of dietary polyphenols. Nutrients. 2010; 2(12): 1231-1246.
12 Lattimer, J.M., Haub,M.D. Effects of Dietary Fiber and Its Components on Metabolic Health. Nutrients . 2010 Dec; 2(12): 1266–1289.
13 Simpson, H.L., Campbell, B.J. Review article: dietary fibre-microbiota interactions. Aliment Pharmacol Ther. 2015 Jul; 42(2):158-179.
14 Goldsmith, J.R., Sartor, R.B.. The role of diet on intestinal microbiota metabolism: downstream impacts on host immune function and health, and therapeutic implications. J Gastroenterol. 2014 May; 49(5):785-798.
15 Tan, J., McKenzie, C., Potamitis, M., Thorburn, A.N., Mackay, C.R., Macia, L. The role of short-chain fatty acids in health and disease. Adv Immunol. 2014; 121:91-119.
16 Conlon, M.A., Bird, A.R. The Impact of Diet and Lifestyle on Gut Microbiota and Human Health. Nutrients. 2015 Jan; 7(1): 17–44.
17 Pagliaro, B., Santolamazza, C., Simonelli, F., Rubattu, S. Phytochemical Compounds and Protection from Cardiovascular Diseases: A State of the Art. Biomed Res Int. 2015; 2015: 918069. Published online 2015 Oct 4.
18 Yang, L., Zhang, J., Yan, C..SIRT1 regulates CD40 expression induced by TNF-α via NF-κB pathway in endothelial cells. Cellular Physiology and Biochemistry. 2012; 30(5):1287–1298.
19 Liu, Y., Ma, W., Zhang, P., He, S., Huang, D. Effect of resveratrol on blood pressure: a meta-analysis of randomized controlled trials. Clinical Nutrition. 2015; 34(1):27–34.
20 Lan, J., Zhao, Y., Dong, F. Meta-analysis of the effect and safety of berberine in the treatment of type 2 diabetes mellitus, hyperlipemia and hypertension. Journal of Ethnopharmacology. 2015; 161:69–81.
21 Yashiro, T., Nanmoku, M., Shimizu, M., Inoue, J., Sato, R. Resveratrol increases the expression and activity of the low density lipoprotein receptor in hepatocytes by the proteolytic activation of the sterol regulatory element-binding proteins. Atherosclerosis. 2012; 220(2):369–374.
22 Lasa, A., Schweiger, M., Kotzbeck, P. Resveratrol regulates lipolysis via adipose triglyceride lipase. Journal of Nutritional Biochemistry. 2012; 23(4):379–384.
23 Gurusamy, N., Lekli, I., Mukherjee, S. Cardioprotection by resveratrol: a novel mechanism via autophagy involving the mTORC2 pathway. Cardiovascular Research. 2010; 86(1):103–112.
24 Zordoky, B.N., Robertson, I.M., Dyck ,J.R. Preclinical and clinical evidence for the role of resveratrol in the treatment of cardiovascular diseases. Biochimica et Biophysica Acta. 2014; 1852(6):1155–1177.
25 Murashima, M., Watanabe, S., Zhuo, X.-G., Uehara, M., Kurashige, A. Phase 1 study of multiple biomarkers for metabolism and oxidative stress after one-week intake of broccoli sprouts. BioFactors. 2004; 22(1–4):271–275.
26 Wang, Y., Huang, Y., Lam, K S L. Berberine prevents hyperglycemia-induced endothelial injury and enhances vasodilatation via adenosine monophosphate-activated protein kinase and endothelial nitric oxide synthase. Cardiovascular Research. 2009; 82(3):484–492.
27 Carrizzo, A., Puca, A., Damato, A. Resveratrol improves vascular function in patients with hypertension and dyslipidemia by modulating NO metabolism. Hypertension. 2013; 62(2):359–366.
28 Magyar, K., Halmosi, R., Palfi, A. Cardioprotection by resveratrol: a human clinical trial in patients with stable coronary artery disease. Clinical Hemorheology and Microcirculation. 2012; 50(3):179–187.
29 Bhatt, J.K., Thomas, S., Nanjan, M.J. Resveratrol supplementation improves glycemic control in type 2 diabetes mellitus. Nutrition Research. 2012; 32(7):537–541.
30 Militaru, C., Donoiu, I., Craciun, A., Scorei, I.D., Bulearca, A.M., Scorei, R. I. Oral resveratrol and calcium fructoborate supplementation in subjects with stable angina pectoris: effects on lipid profiles, inflammation markers, and quality of life. Nutrition. 2013; 29(1):178–183
31 Méndez-del Villar, M., González-Ortiz, M., Martínez-Abundis, E., Pérez-Rubio, K.G., Lizárraga-Valdez, R. Effect of resveratrol administration on metabolic syndrome, insulin sensitivity, and insulin secretion. Metabolic Syndrome and Related Disorders. 2014; 12(10):497–501
32 Bahadoran, Z., Mirmiran, P., Hosseinpanah, F., Rajab, A., Asghari, G., Azizi, F. Broccoli sprouts powder could improve serum triglyceride and oxidized LDL/LDL-cholesterol ratio in type 2 diabetic patients: a randomized double-blind placebo-controlled clinical trial. Diabetes Research and Clinical Practice. 2012; 96(3):348–354.
33 Jennings, A., Welch, A.A., Fairweather-Tait, S.J. Higher anthocyanin intake is associated with lower arterial stiffness and central blood pressure in women. The American Journal of Clinical Nutrition. 2012; 96(4):781–788.
34 Soni, K.B., Kuttan, R. Effect of oral curcumin administration on serum peroxides and cholesterol levels in human volunteers. Indian Journal of Physiology and Pharmacology. 1992; 36(4):273–275.
35 Alwi, I., Santoso, T., Suyono, S.. The effect of curcumin on lipid level in patients with acute coronary syndrome. Acta Medica Indonesiana. 2008; 40(4):201–210.
36 Affuso, F., Ruvolo, A., Micillo, F., Saccà, L., Fazio, S. Effects of a nutraceutical combination (berberine, red yeast rice and policosanols) on lipid levels and endothelial function randomized, double-blind, placebo-controlled study. Nutrition, Metabolism and Cardiovascular Diseases. 2010; 20(9):656–661.
37 Slavin, J. Fiber and Prebiotics: Mechanisms and Health Benefits. Nutrients. 2013 Apr; 5(4): 1417–1435.
38 Sender, R., Fuchs, S., Milo,R. Are We Really Vastly Outnumbered? Revisiting the Ratio of Bacterial to Host Cells in Humans. Cell, 2016; 164 (3): 337
39 Slavin, J.L. Position of the American Dietetic Association: Health implications of dietary fiber. J. Am. Diet. Assoc. 2008; 108:1716–1731.
40 Tucker, L..A., Thomas, K.S. Increasing total fiber intake reduces risk of weight and fat gains in women. J. Nutr. 2009; 139:576–581.