PDGF Signaling And Obesity

Here is a study suggesting that Platelet-derived growth factors and signaling related to that factors plays an important role in obesity by promoting blood vessel growth associated with “white fat” – thus promoting obesity and subsequent obesity-related disorders.  Abstract:

Platelet-derived growth factor (PDGF) is a key factor of angiogenesis; however, its role in adult obesity remains unclear. In order to clarify its pathophysiological role, we investigated the significance of a PDGF receptor β on adipose tissue expansion and glucose metabolism. Mature vessels in the epididymal white adipose tissue (eWAT) were tightly wrapped with pericytes in normal mice. Pericytes desorption from vessels and the subsequent proliferations of endothelial cells were markedly increased in the eWAT of diet-induced obese mice. Analyses with flow cytometry and adipose tissue cultures indicated that PDGF-B caused the detachment of pericytes from vessels in a concentration-dependent manner. M1-macrophages were a major type of cells expressing PDGF-B in obese adipose tissue. In contrast, pericyte detachment was attenuated and vascularity within eWAT was reduced in tamoxifen-inducible conditional Pdgfrb-knockout mice with decreases in adipocyte size and chronic inflammation. Furthermore, Pdgfrb-knockout mice showed enhanced energy expenditure. Consequently, diet-induced obesity and the associated deterioration of glucose metabolism in wild-type mice were absent in Pdgfrb-knockout mice. Therefore, PDGF-B-PDGFRβ signaling plays a significant role in the development of adipose-tissue neovascularization, and appears to be a fundamental target for the prevention of obesity and type 2 diabetes.

Note the last sentence.  One assumes that this signaling can be at some point targeted by drugs, but one can also assume side-effects (never mind cost).  Maybe it would be better to control obesity through diet?  Note in the study, obesity in the mice was “diet-induced.”  That says something, doesn’t it? Diet or drugs?  I’ll pick diet.

Exercise And Brown fat

More inert white adipose tissue (WAT) is linked to a variety of obesity-related disorders, as opposed to the more metabolically active brown fat.  It's possible to "remodel" WAT to make it more active, a process called "browning." Not surprisingly, exercise training has been shown to promote "browning" as discussed here. abstract:

Exercise training increases the thermogenic capacity of white adipose tissue (WAT), an effect known as "browning" of the WAT. Here, we discuss how this affects whole-body energy homeostasis. We put forth the hypothesis that browning of the subcutaneous WAT allows the organism to adjust its metabolic rate according to energy availability while coping with increased heat production through exercise.

Yet another benefit of physical activity/exercise.

High Fat Diet And the Aging Mouse Brain

A high fat diet seems not to be very good for aging of the mouse brain.  Fasting and a low fat diet seemingly have different effects.  Abstract:

Fasting may be exploited as a possible strategy for prevention and treatment of several diseases such as diabetes, obesity, and aging. On the other hand, high-fat diet (HFD) represents a risk factor for several diseases and increased mortality. The aim of the present study was to evaluate the impact of fasting on mouse brain aging transcriptome and how HFD regulates such pathways. We used the NCBI Gene Expression Omnibus (GEO) database, in order to identify suitable microarray datasets comparing mouse brain transcriptome under fasting or HFD vs aged mouse brain transcriptome. Three microarray datasets were selected for this study, GSE24504, GSE6285, and GSE8150, and the principal molecular mechanisms involved in this process were evaluated. This analysis showed that, regardless of fasting duration, mouse brain significantly expressed 21 and 30 upregulated and downregulated genes, respectively. The involved biological processes were related to cell cycle arrest, cell death inhibition, and regulation of cellular metabolism. Comparing mouse brain transcriptome under fasting and aged conditions, we found out that the number of genes in common increased with the duration of fasting (222 genes), peaking at 72 h. In addition, mouse brain transcriptome under HFD resembles for the 30% the one of the aged mice. Furthermore, several molecular processes were found to be shared between HFD and aging. In conclusion, we suggest that fasting and HFD play an opposite role in brain transcriptome of aged mice. Therefore, an intermittent diet could represent a possible clinical strategy to counteract aging, loss of memory, and neuroinflammation. Furthermore, low-fat diet leads to the inactivation of brain degenerative processes triggered by aging.

One can speculate about the human situation.

Cancer Stem Cells And Lipid Metabolism

Cancer stem cells are highly dependent upon lipid metabolism; abstract:

Cancer stem cells (CSCs) are an uncommon subset of tumor cells capable of self-renewal, differentiating, and recreating the parental tumor when transplanted into the murine background. Over the past two decades, efforts toward understanding CSC biology culminated into identifying a set of signaling pathways sustaining "stemness". Nevertheless, while metabolic rewiring is nowadays considered a hallmark of cancer, no consensus has been reached on the metabolic features underlying the plastic nature of CSCs, which are capable of residing in a dormant state, and able to rapidly proliferate when the need to repopulate the tumor mass arises. An emerging concept in the field of CSC metabolism is that these cells are extremely reliant on the activity of enzymes involved in lipid metabolism, such as stearoyl-CoA desaturase 1 (SCD1) and 3-hydroxy-3-methylglutharyl-coenzyme A reductase (HMG-CoAR). Indeed, SCD1 and HMG-CoAR have been described as key factors for the correct function of a number of concatenated pathways involved in CSC fate decision, such as Hippo and Wnt. In the present review, we describe metabolic futures of CSCs with a special focus on lipid metabolism, which until now represents an underappreciated force in maintaining CSCs and an attractive therapeutic target.

Besides being a potential therapeutic target one can speculate if this is involved – even if indirectly – in the link between obesity and cancer.

Don’t Blame Your Genes

It’s not your genes, it’s your appetite and eating habits.

But weight loss averaged about 13 pounds over a year, regardless of genes, insulin levels or diet type. Also, some people lost as much as 60 pounds and others gained 15 pounds — more evidence that genetic characteristics and diet type appeared to make no difference.

What seemed to make a difference was healthful eating. Participants on both diets who consumed the fewest processed foods, sugary drinks, unhealthy fats and ate the most vegetables lost the most weight.

The results suggest that "precision medicine is not as important as eating mindfully, getting rid of packaged, processed food" and avoiding unhealthy habits like eating while watching television, said lead author Christopher Gardner.

So, excuses about “it’s my genes” do not justify BMI realities, and fad diets are a waste of time, if key essentials are met: “Participants on both diets who consumed the fewest processed foods, sugary drinks, unhealthy fats and ate the most vegetables lost the most weight."

I for one cut out sugary drinks – including orange juice and other fruit juices – cut back on saturated fats, cut back on foods with lots of added sugar, eat a bit less “packaged food,” while increasing fruits, vegetables, and whole grain as opposed to white.

Yaks And The Fat Cells

By Dennis Jarvis, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=22519671

Of possible future relevance to humans, how adipocyte (fat cell) differentiation is controlled in the domestic yak. Abstract:

The domestic yak (Bos grunniens) is a culturally important animal that lives at high altitude and is farmed by Tibetan herders for its meat, milk, and other animal by-products. Within the animal, adipose tissue is an important store and source of energy and is used to maintain adequate body temperature during the extended cold seasons. Exploring the biomolecular role of microRNAs (miRNAs) in the regulation of growth, development, and metabolism of yak adipocytes may provide valuable insights into the physiology of adipogenesis in the yak. This study investigated whether and how miR-200a (a miRNA recently reported to promote adipogenesis in ST2 bone marrow stromal cells) regulates adipocyte differentiation in the yak. Expression levels of miR-200a gradually increased during day 0 to day 8 of adipocyte differentiation, and transfection of adipocytes with miR-200a enhanced lipid accumulation and triglyceride content compared to control (un-transfected) adipocytes. We additionally verified (using qRT-PCR analysis) that miR-200a increased the expression of adipocyte-specific genes involved in lipogenic transcription (PPARγ, ELVOL, and C/EBPα), fatty acid synthesis (ACC, ACS, SCD, and FAS), and fatty acid transport (DGAT, LPL, and FABP4). We also found that transfection of adipocytes with miR-200a resulted in suppression of the levels of noncanonical Wnt signaling transcription factors (Wnt5a, TAK1, and NLK). These results indicate that miRNA-200a plays an important role in promoting yak adipocyte differentiation that may operate via the suppression of noncanonical Wnt signaling.

Fat Tails And Cell Signaling

Cell signaling pathways responsible for fat deposition have been studied in fat-tailed sheep, a breed characterized by an appearance associated with its name.  These findings may have relevance to the human condition.  Of course, the major reasons for fat deposition in humans is diet and inactivity, but research into the problem can be useful.  Abstract:

Adipose tissues are phenotypically, metabolically and functionally heterogeneous based on the sites of their deposition. Undesirable fat deposits in the body are often detrimental to animal and human health. To unravel the potential underlying mechanisms governing accumulation of adipose tissues in various regions of the body, i.e., subcutaneous (SAT), visceral (VAT) and tail (TAT), we profiled transcriptomes from Tan sheep, a Chinese indigenous breed with notable fat tail using RNA-seq. Upon comparison, we identified a total of 1,058 differentially expressed genes (DEGs) between the three adipose types (218, 324, and 795 in SAT/VAT, SAT/TAT, and VAT/TAT, respectively), from which several known key players were identified that are involved in lipid metabolic process, Wnt signals, Vitamin A metabolism, and transcriptional regulation of adipocyte differentiation. We also found that many elevated genes in VAT were notably enriched for key biological processes such as cytokine secretion, signaling molecule interaction and immune systems. Several developmental genes including HOXC11, HOXC12 and HOXC13, and adipose-expressed genes in the tail region, such as HOTAIR_2, HOTAIR_3 and SP9 were specially highlighted, indicating their strong associations with tail fat development in fat-tailed sheep. Our results provide new insight into exploring the specific fat deposition in tail, also contribute to the understanding of differences between adipose depots.

Obesity, Hypoxia, And Breast Cancer

Public Domain, https://commons.wikimedia.org/w/index.php?curid=1273807

Hypoxia – oxygen deprivation – in tumor tissue can promote cancer development, including breast cancer.  A factor stimulated by hypoxia can affect metastasis through neovascularization (new blood vessel formation).  Obesity can increase hypoxia in adipocytes (fat cells), promoting a favorable environment for tumor cells in breast fat tissue; adipocytes have been shown to enhance expression of the aforementioned factor that promotes blood vessel formation for tumors. More evidence showing the consequences of the obesity epidemic, and the consequences of the media effort to normalize obesity.  Abstract:

OBJECTIVE:The development of breast cancer cells is linked to hypoxia. The hypoxia-induced factor HIF-1α influences metastasis through neovascularization. Hypoxia seems to decrease the responsiveness to hormonal treatment due to loss of estrogen receptors (ERs). Obesity is discussed to increase hypoxia in adipocytes, which promotes a favorable environment for tumor cells in mammary fat tissue, whereas, tumor cells profit from good oxygen supply and are influenced by its deprivation as target regions within tumors show. This review gives an overview of the current state on research of hypoxia and breast cancer in human adipose tissue.METHODS:A systematic literature search was conducted on PubMed (2000-2016) by applying hypoxia and/or adipocytes and breast cancer as keywords. Review articles were excluded as well as languages other than English or German. There was no restriction regarding the study design or type of breast cancer. A total of 35 papers were found. Eight studies were excluded due to missing at least two of the three keywords. One paper was removed due to Russian language, and one was dismissed due to lack of adherence. Seven papers were identified as reviews. After applying exclusion criteria, 18 articles were eligible for inclusion.RESULTS:Two articles describe the impairment of mammary epithelial cell polarization through hypoxic preconditioning. A high amount of adipocytes enhances cancer progression due to the increased expression of HIF-1α which causes the loss of ER α protein as stated in four articles. Four articles analyzed that increased activation of HIF's induces a series of transcriptions resulting in tumor angiogenesis. HIF inhibition, especially when combined with cytotoxic chemotherapy, holds strong potential for tumor suppression as stated in further four articles. In two articles there is evidence of a strong connection between hypoxia, oxidative stress and a poor prognosis for breast cancer via HIF regulated pathways. Acute hypoxia seems to normalize the microenvironment in breast cancer tissue and has proven to affect tumor growth positively as covered in two articles.CONCLUSION:This review indicates that the development of breast cancer is influenced by hypoxia. A high amount of adipocytes enhances cancer progression due to the increased expression of HIF-1α.

Molecular Pathway Linking Colon Cancer To A High Fat Diet (And Obesity)

By Attributed to Charles Mellin - WgF1LrUvFdNysA at Google Cultural Institute, zoom level maximum, Public Domain, https://commons.wikimedia.org/w/index.php?curid=13334241

A study has shown a molecular pathway linking obesity and a high fat diet to colon cancer.  Excerpts from the article (italics) with some of my own comments inserted:

Scientists in the U.S. have identified a molecular pathway that appears to play a key role in the link between a high-fat diet (HFD) and the development of colorectal cancer. The research, led by the Cleveland Clinic’s Sheerlarani Karunanithi, and Matthew Kalady, suggests that it may one day be possible to develop drugs that reduce tumor growth associated with obesity and a diet that is high in fat. 

Or people can lose weight and eat lower-fat diets.  What's wrong with that approach?

Their research is published today, in Stem Cell Reports, in a paper titled, “RBP4-STRA6 Pathway Drives Cancer Stem Cell Maintenance and Mediates High-Fat Diet-Induced Colon Carcinogenesis.”

The Cleveland Clinic team’s review of published research indicated that high expression levels of two vitamin A signalling proteins—serum retinol binding protein (RPB4), stimulated by retinoic acid 6 (STRA6)—in colorectal cancer tumors is associated with poor prognosis, increased tumor metastasis and recurrence, and resistance to cancer therapy. The RBP4-STRA6 pathway triggers the JAK2-STAT3 signaling cascade…

That is useful information - perhaps the greatest utility is motivation to lose wright and change diets, as there is now more concrete evidence linking unhealthy eating habits and an unhealthy weight to colon cancer.

...Our data clearly indicate that RBP4-STRA6 pathway is necessary for the optimal expression of stem cell markers such as NANOG, SOX2, and LGR5, and thereby for maintaining the colon CSC pool,” the authors conclude in their published paper. "We have known the influence of diet on colorectal cancer,” commented Matthew Kalady, M.D., colorectal surgeon, and co-director of the Cleveland Clinic Comprehensive Colorectal Cancer Program. “However, these new findings are the first to show the connection between high-fat intake and colon cancer via a specific molecular pathway. We can now build upon this knowledge to develop new treatments aimed at blocking this pathway and reducing the negative impact of a high-fat diet on colon cancer risk."

One could reasonably reduce the risk of a high-fat diet by no longer eating the high-fat diet.

“The interesting finding here is that the high fat diet-induced effects appear to also involve the stem cell program, which is interesting for tumor growth and has implications on therapies, as tumor stem cells are also therapeutically resistant...” 

It would seem therefore if high-fat diets maintain colon cancer stem cells - cells that can "fuel" the tumor and which may be more resistant to therapy - then one can ask: should colon cancer patients be given nutritional programs that take this into account?

There's nothing wrong with developing new therapies, but those therapies should be in addition to healthy eating, not a substitute for it.

More Against Red And Processed Meat

By 4028mdk09 - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=25399566

Is enhanced mortality associated more with red meat/processed meat consumption or with saturated fatty acid (SFA) consumption?  Is it the meat or the saturated fats?  A recent study says meat:

Among highly educated persons, aged >45 years, a high consumption of red, total, and red + processed meat was related to increased all-cause mortality, compared with those with low consumption, whereas no significant associations were found for SFA intake. Dietary guidelines should specifically limit meat consumption and not relying only in limiting SFA intake.

And:

…replacing 100 g of vegetables, fruits & nuts or cereals by 100 g of red meat resulted in higher mortality risk.

For older individuals eating more meat, there was some effect of more SFA consumption:

In these participants, SFA intake was non-significantly associated with mortality. However, isocaloric replacement of monounsaturated fat or carbohydrates by SFA resulted in significantly higher mortality risk. 

But overall this particular study provides data pointing the finger at red meat/processed meat.  Given the consistency of this finding with that of previous studies, it looks for now that excessive consumption of red meat/processed meat is a major dietary health risk.  Looking at all studies, SFA risk is more equivocal; this study does not show, overall, a significant risk, but other studies have showed such a risk.

Limiting red meat/processed meat consumption would seem to be a prudent dietary priority.  Limiting SFA may be a good idea as well, depending upon context and whatever other dietary recommendations a person has from their physician, etc., but the meat situation would seem more important at this point.  Who knows what further studies will say about SFA.

Fat, Leptin, Mice, And Colon Cancer

By The original uploader was Bigplankton at English Wikipedia Later versions were uploaded by Sunholm at en.wikipedia. - Human Genome wall for SC99 on ornl.gov. Copied from en.wikipedia; description page is/was here., Public Domain, https://commons.wikimedia.org/w/index.php?curid=1777620 

This study used mice that model colon cancer induced by azoxymethane and dextran sulfate sodium. 

The mice were fed a regular diet or a high-fat diet (HFD), and the researchers found that the HFD-fed mice had more colon inflammation, more tumors, and different gene expression compared to regular-diet mice.  

Some of the changes in the HFD mouse colon were similar to these found in human colon cancer, particularly colon cancer with inflammatory microsatellite instability.  

Leptin and Wnt signaling were altered in the HFD mice, and such alterations are also associated with colon cancer. Upregulation of the leptin pathway is associated with worse overall survival; whereas, Wnt signaling deregulation is often the initiating step in the development of colon cancer.

Taking into account the similarities to the human colon cancer, the importance of diet becomes clear.

Going Nuts for Heart Health

When I was young, the paradigm was ‘fat is fat”, and all forms of fat were to be reduced to the absolute minimum. That led to a carbohydrates - heavy diet which likely has contributed to today’s epidemic of obesity, metabolic syndrome, and type 2 diabetes. Today, our current understanding is that unsaturated fats, in moderation, can be healthy. Thus, nuts, one forbidden as a “fat food,” are now considered healthy, if consumed in moderation, and as part of an overall healthy diet.
 

Eating nuts as part of a healthy diet can be good for your heart. Nuts, which contain unsaturated fatty acids and other nutrients, are a great snack food, too. They're inexpensive, easy to store and easy to pack when you're on the go.
 
The type of nut you eat isn't that important, although some nuts have more heart-healthy nutrients and fats than do others. Walnuts, almonds, hazelnuts — you name it — almost every type of nut has a lot of nutrition packed into a tiny package. If you have heart disease, eating nuts instead of a less healthy snack can help you more easily follow a heart-healthy diet.
 
Can eating nuts help your heart?
 
People who eat nuts as part of a heart-healthy diet can lower the low-density lipoprotein (LDL, or "bad") cholesterol level in their blood. High LDL is one of the primary causes of heart disease.
 
Eating nuts may reduce your risk of developing blood clots that can cause a fatal heart attack.
 

Once again, moderation is key.

 As much as 80 percent of a nut is fat. Even though most of this fat is healthy fat, it's still a lot of calories. That's why you should eat nuts in moderation. Ideally, you should use nuts as a substitute for saturated fats, such as those found in meats, eggs and dairy products. 

Instead of eating unhealthy saturated fats, try substituting these with a handful of nuts or a tablespoon or two of a nut spread. The American Heart Association recommends eating four servings of unsalted nuts a week. Select raw or dry-roasted nuts rather than those cooked in oil.

A serving is a small handful (1.5 ounces) of whole nuts or 2 tablespoons of nut butter. But again, do this as part of a heart-healthy diet. Just eating nuts and not cutting back on saturated fats found in many dairy and meat products won't do your heart any good.

Eating some walnut or almonds, or having a couple of tablespoons of peanut butter or almond butter can therefore constitutes a tasty part of a heart-healthy diet.

Check these recipes for walnut-chocolate clusters and spicy walnuts.

Eat Your Walnuts

It’s time to eat some walnuts!

When people in the study added 56 grams of walnuts (2 ounces, or about 14 walnuts) to their daily diet for six months, they improved blood vessel function and reduced “bad” LDL cholesterol that builds up in blood vessels and leads to blood clots and heart attacks.

“Adding walnuts to your diet will improve your diet quality and health – cardiometabolic health specifically – and you can add walnuts without fear of weight gain because they are very satiating and appear to bump out other calories quite reliably and make room for themselves,” said study author Dr. David L. Katz of the Yale University Prevention Research Center in Derby, Connecticut.

Walnuts of course cannot help with everything: 

The nuts didn’t seem to improve high blood pressure and high blood sugar, two other risk factors for diabetes, Katz and colleagues reported in BMJ Open Diabetes Research and Care.

Which is why walnut consumption needs to be part of an overall healthy diet. 

After taking into account factors such as age, exercise habits, calorie consumption and fatty acid intake, the study found that walnuts were linked to improved diet quality regardless of whether people received nutrition counseling.

Please keep in mind this: 

The California Walnut Commission funded the study and has compensated Katz for speaking engagements.

One limitation of the research is that participants weren’t given specific foods to consume and diets were assessed based on self-reported surveys asking people at several points to recall what they ate in the previous 24 hours, the authors acknowledge. The study also wasn’t designed to show whether walnuts could prevent diabetes, which makes the results less reliable.

Even though the data from the study suggest that adding walnuts to the diet can help maintain overall healthy eating habits, more research from larger and longer-term studies is still needed to fully understand the potential benefits of walnuts, said Roberta Holt, a nutrition researcher at the University of California, Davis, who wasn’t involved in the study. Results from the periodic diet surveys aren’t enough to prove walnuts caused the changes in LDL cholesterol or blood vessel function, Holt added by email.

“While the intake of walnuts improved LDL cholesterol and vascular function from baseline, the control (no walnuts) also improved,” Holt noted.

Actionable

There is plenty of research linking consumption of walnuts to improved markers of heart health and lower risks of diabetes and heart disease. Deirdre Tobias, an epidemiologist at Brigham and Women’s Hospital and Harvard Medical School in Boston noted that “Walnuts and other tree nuts are a healthful source of plant-based protein and fat,” and “They are a food that (is) consistent with overall dietary recommendations and can easily be incorporated into a patient’s diet, if they like walnuts and are not allergic.”

Addictive Foods?

A study has investigated which types of food are most addictive. The results are not surprising:

For the first time, a team of researchers looked at exactly which types of foods could be the most addictive. They asked a group of 120 undergraduates at the University of Michigan, and another group of nearly 400 adults, about 35 different types of food -- from pizza to broccoli -- and whether they think they could have problems controlling how much they ate of each one. Eighteen of the items were processed foods, meaning they contained added sugars and fats.
 
Topping the list were pizza, chocolate, chips, cookies, ice cream, French fries, cake and soda, all considered processed foods. They were followed by cheese and bacon -- both unprocessed foods, but high in fat and salt.
 
The researchers found that the most problematic foods tended to be those with a high glycemic load, meaning they contained a lot of sugar and caused a spike in blood sugar. The authors wrote that these qualities could make foods more difficult to stop eating in a similar way as drugs that are highly concentrated and rapidly absorbed into the body are more addictive.
 
The researchers also found that, among the adults in their study, those with a high BMI and those who were at risk of having any kind of food addiction were most likely to have difficulty controlling themselves around a particular food item.
Note that this article considers bacon to be an “unprocessed food” defining such as having “added sugars and fats” while bacon is typically considered to be a processed food.
The take home message is that foods that are less healthy choices are those which are most addictive, and those two characteristics are linked. Sugar, fat, and salt promote cravings, and at the same time, these components have the worst nutritional profile. Further, those most at risk for food-related health problems, such as individuals with a high BMI, are more likely to have problems with food addiction.

It is important to try to break the vicious cycle of eating these foods, craving more, and eating more. In theory, if you have never eaten these foods, and avoid being exposed to them, you won’t develop the addiction. This is unrealistic since almost all of us, myself included, have consumed these foods many times at one point or another in our lives. So, you need to make a conscious decision to resist: avoid eating out, do not buy these items, and eat healthier at home. The good news is that with time, your tastes will adapt. After ditching foods like Pop Tarts for fresh fruit, I have found that the fruit tastes sweeter to me than it did before, when I was routinely exposed to high-sugar, highly processed food.
It is important not to be obsessed with food, not to use food as some sort of “comfort” or “drug” in response to stressors and problems. Certainly, you should enjoy what you eat, and once you adjust to a healthier diet, you will find out that you enjoy the healthy foods more, and the types of foods you ate in the past taste “too rich.” So, yes, healthy food can and should be palatable. However, do not make food a focus of your life, so that avoiding unhealthy and addictive foods would not feel like a sacrifice. Once you have a healthy food regimen in place, you could have “cheat meals” infrequently – the occasional slice of pizza, a piece of chocolate, or a Pop Tart, or even that dreaded slice of bacon.
Actionable
You need to make the commitment that your relationship with food will change. The primary function of food is to be fuel for your body and to improve your health. Food consumption cannot be a major focus in your life, food cannot be a drug to distract you from life’s problems.

Fructose - Your Foe

We all know that sugar is bad for us. This is why the World Health Organization recommends us to limit our sugar (sucrose) intake to six teaspoons a day. But did you know that fructose, one of the individual types of sugar, is toxic for you? You may not be aware that you consume fructose every day. It is present in regular sugar “sucrose” (composed by glucose and fructose at a ratio of 1:1); however, its main source in the diet is the omnipresent high fructose corn syrup. This “syrup” is added to almost everything: from soft drinks, candy, bread, to tomato soup and ketchup. It is even in some potato and macaroni salads in the neighborhood deli. The fruit juices also contain considerable levels of fructose.
 
Whereas the sugar glucose is used as an energy source by every single cell in the body, fructose is not. Be aware, however, that excess of glucose intake could be converted into fructose in the body. Unlike glucose, fructose can be utilized only by liver cells, where fructose processing results in increased levels of the toxic uric acid and fat. Thus, excess of fructose intake from the diet results in excess fat in the liver (and “fatty liver” disease) and excess fat circulating in the blood. The increased fat in the blood accumulates in the body, and leads to obesity, cardiovascular (heart) diseases, and type 2 diabetes. In fact, fructose is the main culprit for metabolic syndrome, the condition in which high blood pressure, high blood sugar, excess body fat around the waist, and high cholesterol levels co-occur.


Actionable

• Read the ingredients of each food product in your refrigerator and pantry. If “high fructose corn syrup” is one of the ingredients, discard the product. Stop buying such products.

• Stop drinking soft drinks and fruit juices. Instead, eat fruit and drink water.

• Do not allow your children to drink anything else but water and plain milk.

• Laugh with this Coca Cola video. Coca Cola is one of the companies that have drowned us in drinks with high fructose corn syrup and sugar.

• Next time you want to eat out, think twice: do you know what is in your meal? The only way to be sure is to cook it yourself. Learn how to cook with these affordable recipes from the free Good and Cheap cookbook.

• If you do eat out and you are served in a plate larger than 9 inches in diameter, chances are that there is too much food. Eat only half of the meal and take the other half home.