Saturday, November 16, 2019

Too many chemicals in Our Foods

Hyper Palatable Foods that People Can’t Stop Eating
November 16, 2019 Don Porter
Hyper-palatable foods are those made with a mix of ingredients/chemicals that light up people’s brain-reward neural circuitry and overpower mechanisms that are supposed to signal when we’ve had enough to eat. Because these foods essentially enhance their consumption, overweight and obesity can be the result. Of 84,000 chemicals listed only an estimates 30,000 are actually in use 2019. This class of foods which are often processed foods or sweets containing alluring combinations of sugar, fat, sodium and carbohydrates, have been found to be some of the most highly consumed foods in the United States. Food companies have devised formulas for these foods to make them highly palatable and thus enhance their consumption. TOO MANY foods are made to Look good, Smell good, Taste good, Be addictive, and Last a Long time !  All done with use of MANY chemicals !!
While there is no standardized definition for hyper palatable foods, typically descriptive definitions such as “desserts”, “fast foods” and “sweets” will identify these types of foods. However, those words aren’t specific to the actual mechanisms through which the ingredients in a particular food lead to their enhanced palatability. Defining these types of foods has been a substantial limitation.
A team sought to define the criteria for hyper palatable foods through conducting a literature review and then employing nutrition software and applying their definition to over 7,700 food items. They essentially took all the descriptive definitions of these foods from the literature and one by one entered them into the nutrition program to see how it quantifies a food’s ingredients. The software provides in fine grained detail a data set which specifies how many calories, fat, sodium, sugar, carbohydrates and fiber are in the foods. They looked for items that met the criteria established by the literature review as enhancing palatability and specifically when the synergy between key ingredients in a certain food creates an artificially palatable experience which is larger than any key ingredient would produce by itself.
They identified these particular synergies with specific values which were applied to three clusters – combinations of sodium and fat (such as bacon and hot dogs), combinations of simple sugars and fats (such as ice cream, cookies, and cake), and combinations of sodium and carbohydrates (such as pretzels, chips and popcorn).
Essentially the team wanted to be able to identify foods that seem to cluster together which what seemed like similar levels of at least two ingredients. That is the theoretical basis for producing the synergistic palatability effect. Through a process using visualization, they were able to see there were essentially three food types that appear to cluster together in relation to their ingredients. Once the team was able to quantify characteristics of hyper palatability, they were able to apply their definition to foods that are cataloged in the U. S. Dep of Agriculture’s FNDDS (Food and Nutrient Database for Dietary Studies). The hope was to discover just how prevalent these types of foods are in the hope was in our diets.
The team discovered that 62% of foods in the FNDDS met the criteria for at least one of the three clusters they had identified. Most of those foods (70%) were high in sodium and fat (such as egg or meat dishes and milk based foods like cheese dips). 25% of the hyper palatable foods were high in sugar and fat and 16% of those foods were also high in sodium and carbohydrates. Less than 10% qualified in more than one cluster.  The most shocking discovery were items labeled as reduced or no fat, salt, sugar or calories represented 5% of hyper palatable foods. Additionally, of all the items that were labeled as low/reduced/no fat, sodium and/or sugar in the FNDDS, 49% met the criteria as a being a hyper palatable food.
·        Palm Oil. ...
·        Shortening. ...
·        White Flour, Rice, Pasta, and Bread. ...
·        High Fructose Corn Syrup, Sugar...
·        Artificial Sweeteners. ...
·        Sodium Benzoate and Potassium Benzoate. ...
·        Butylated Hydroxyanisole (BHA) ...
·        Sodium Nitrates and Sodium Nitrites.

More evidence is needed, however if research starts to support that these hyper palatable foods may be problematic for society, it might warrant food labels saying “this is hyper palatable”. And it might also lead to restriction of certain foods that are available in particular places such as elementary school cafeterias that serve kids whose brains are still developing and might be impacted by these kinds of foods.  The plan is to build on the current work by analyzing how the ubiquity of these hyper palatable foods in the U.S. diet compares to foods in other countries. 

Wednesday, October 23, 2019

Dr. Mercola endorses Baking Soda to fight Cancer

The Role of Fungus in Cancer
Analysis by Dr. Joseph Mercola   October 23, 2019
·                  Research shows fungi can migrate from your gut to your pancreas, where it can contribute to the development of pancreatic cancer. In mouse and human models, pancreatic tumors contain 3,000 times more fungi than normal pancreatic tissue
·                  Pancreatic tumors had far greater amounts of a common fungal genus called Malassezia. Using an antifungal drug was found to be protective, slowing down the progression of the tumor
·                  The fungi trapped in the pancreas appears to drive tumor growth by activating MBL (mannose-binding lectin), a liver protein that triggers an immune mechanism involved in fighting infections
·                  Solid tumors excrete acid and the spread of cancer cells is stimulated by acidic conditions in the surrounding tissues. Acid is a byproduct of glucose metabolism, which ties in with research showing cancer feeds on and is accelerated by a diet high in sugar
·                  Previous research suggests baking soda can be helpful for inhibiting cancer metastasis. It also appears to improve the effectiveness of other cancer treatments
Oftentimes, even the most unlikely-sounding theories can be scientifically validated if you just wait long enough. That certainly rings true for recent headlines declaring fungi and bacteria may be playing a role in the development of certain types of cancer, combined with previous research showing baking soda may be a useful remedy.  In 2011, shamed Dr. Oz for allowing me on his show,1 and one of the "reasons" given was that I had at one time published information about a novel hypothesis — the idea that cancer could be caused by common fungi and might be treatable with baking soda.
Two early proponents of this hypothesis were Tullio Simoncini2,3 and Mark Sircus.4 As you might expect, they were unsuccessful in their attempts at getting the conventional medical establishment to take the hypothesis seriously and have been maligned and marginalized for promoting these ideas.  So, mark my surprise when October 3, 2019, The New York Times published an article5 titled, "In the Pancreas, Common Fungi May Drive Cancer." The article reported the findings of a study6,7 published in the October 2019 issue of the prestigious Nature journal. According to this study:8
"Bacterial dysbiosis accompanies carcinogenesis in malignancies such as colon and liver cancer, and has recently been implicated in the pathogenesis of pancreatic ductal adenocarcinoma (PDA). However, the mycobiome has not been clearly implicated in tumorigenesis.  Here we show that fungi migrate from the gut lumen to the pancreas, and that this is implicated in the pathogenesis of PDA. PDA tumors in humans and mouse models of this cancer displayed an increase in fungi of about 3,000-fold compared to normal pancreatic tissue."
Fungal Microbiome May Play a Role in Pancreatic Cancer
More specifically, the mycobiome (the fungal microbiome) found in pancreatic tumors was distinctly different from the mycobiome found in the gut and in normal pancreases.  According to the researchers, PDA tumors had far greater amounts of a common fungal genus called Malassezia. Killing off the mycobiome with an antifungal drug was found to be protective, slowing down the progression of the tumor. As reported by Medical News Today:9
"The team found that treating mice with a strong antifungal drug called amphotericin B reduced tumor weight by 20–40%. The treatment also reduced ductal dysplasia, an early stage in the development of pancreatic cancer, by 20–30%.  Antifungal treatment also boosted the anticancer power of gemcitabine, a standard chemotherapy drug, by 15–25% …"
On the other hand, repopulating the tumor with Malassezia accelerated tumor growth, except when Candida, Saccharomyces or Aspergillus genera were used. This suggests Malassezia is the main culprit in this kind of cancer. When other genera were included, tumor growth was much slower.
"We also discovered that ligation of mannose-binding lectin (MBL), which binds to glycans of the fungal wall to activate the complement cascade, was required for oncogenic progression, whereas deletion of MBL or C3 in the extratumoral compartment … were both protective against tumor growth," the authors note,10 concluding that:
"Collectively, our work shows that pathogenic fungi promote PDA by driving the complement cascade through the activation of MBL."    In summary, the fungi trapped in the pancreas appears to drive tumor growth by activating MBL (mannose-binding lectin), a liver protein that triggers the complement cascade11 — an immune mechanism involved in fighting infections.    The problem is that this mechanism can also promote the growth of cells after the infection has been resolved.12,13 When MBL activation was inhibited, tumor growth was also inhibited.14
Microenvironment Is an Important Consideration
As reported by The New York Times,15 up until very recently, the pancreas was thought to be a sterile organ, which made these findings all the more surprising. The New York Times goes on to state:
"There is increasing scientific consensus that the factors in a tumor's 'microenvironment' are just as important as the genetic factors driving its growth.  'We have to move from thinking about tumor cells alone to thinking of the whole neighborhood that the tumor lives in,' said Dr. Brian Wolpin, a gastrointestinal cancer researcher at the Dana-Farber Cancer Institute in Boston.   The surrounding healthy tissue, immune cells, collagen and other fibers holding the tumor, as well as the blood vessels feeding it all help support or prevent the growth of the cancer.  Microbes are one more factor to consider in the alphabet soup of factors affecting cancer proliferation. The fungal population in the pancreas may be a good biomarker for who's at risk for developing cancer, as well as a potential target for future treatments.  'This is an enormous opportunity for intervention and prevention, which is something we don't really have for pancreatic cancer,' said Dr. Christine Iacobuzio-Donahue, a pancreatic cancer researcher at Memorial Sloan Kettering in New York."  That this research is being taken seriously is evidenced by its widespread media coverage. As reported in an accompanying article in Nature News and Views:16   "The mycobiome is a historically under-recognized player in human health and disease, but its role in both is essential. Harmless organisms called commensals, including fungi, inhabit mucosal surfaces such as the linings of the gut, nose and mouth, and can activate inflammatory processes as part of the immune system's response to injury or infection …  Moreover, it is becoming apparent that there is a relationship between the gut mycobiome and human cancers, including colorectal and esophageal cancer."
Baking Soda Inhibits Cancer Metastasis
While the featured Nature study did not address the potential use of baking soda (sodium bicarbonate), research17 published in the journal Cancer Research in 2009 did. According to the abstract:18
"The external pH of solid tumors is acidic as a consequence of increased metabolism of glucose and poor perfusion. Acid pH has been shown to stimulate tumor cell invasion and metastasis in vitro and in cells before tail vein injection in vivo.   The present study investigates whether inhibition of this tumor acidity will reduce the incidence of in vivo metastases. Here, we show that oral NaHCO3 selectively increased the pH of tumors and reduced the formation of spontaneous metastases in mouse models of metastatic breast cancer.  This treatment regimen was shown to significantly increase the extracellular pH, but not the intracellular pH, of tumors … NaHCO3 therapy also reduced the rate of lymph node involvement, yet did not affect the levels of circulating tumor cells, suggesting that reduced organ metastases were not due to increased intravasation.   In contrast, NaHCO3 therapy significantly reduced the formation of hepatic metastases following intrasplenic injection, suggesting that it did inhibit extravasation and colonization."  The authors point out that the extracellular pH of malignant tumors typically ranges between 6.5 and 6.9, whereas normal tissues have an alkaline pH typically ranging between 7.2 and 7.5.    They also cite previous studies showing solid tumors excrete acid and that the spread of cancer cells is stimulated by acidic conditions in the surrounding tissues. The paper also points out that "acid is a byproduct of glucose metabolism," which ties in with research showing cancer feeds on and is accelerated by a diet high in sugar.
In this experiment, mice injected with cancer cells were given either plain drinking water or water with 200 mmol/L bicarbonate. Calculations suggest the equivalent dose in human terms would be 12.5 grams (0.4 ounces) of bicarbonate per day for an individual weighing 154 pounds or 70 kilos. While the bicarbonate therapy had no effect on the rate of growth of the primary tumors, it did significantly reduce the number and size of metastatic tumors in the lungs, intestines and diaphragms, which in turn resulted in improved survival. According to the authors:19    "In the 30-day experiment, pooled data showed that the bicarbonate-treated mice had a total of 147 metastatic lung lesions, whereas the control group had 326 lung lesions. The average lesion diameters were 4.5 ± 0.12 and 5.2 ± 0.14 mm in the NaHCO3 and control groups, respectively."
Baking Soda Might Not Be as 'Quack' as You Thought
In 2012, Mark "Marty" Pagel Ph.D., associate professor of biomedical engineering at the University of Arizona, was given a $2 million grant to investigate whether drinking baking soda water might help patients with breast cancer.20,21   Interestingly, while the use of baking soda in the treatment of cancer has been written off as the worst possible type of quackery by skeptics and critics, the University of Arizona Cancer Center has actually been studying its use for nearly two decades. As reported by Cancer Active in 2017:22    "… in 2003 (Raghunand) they showed how drinking sodium bicarbonate resulted in the alkalization of the area around cancer tumors resulting in a cessation of new metastases23 …
Further research has shown that sodium bicarbonate had an effect on breast and prostate cancers but had mixed results with other cancers … 2009, Robey et al showed that drinking sodium bicarbonate caused new metastases to stop, whilst injection of Bicarbonate into tumors caused regression of the cancer24 …   Ed: At CANCERactive we have a simple view that is identical to that of American cancer researcher Ralph Moss. This is research every cancer patient should know about. If drinking sodium bicarbonate can restrict cancer metastases then it should be considered as a part of an Integrated Cancer Treatment Programme, especially if it enhances the action of chemotherapy drugs."   While Pagel's team has published a number of studies since then, including one detailing the ways in which extracellular pH can be assessed inside in vivo tumors,25,26 they've not yet published anything discussing the use of baking soda as an adjunct to breast cancer treatment.
Baking Soda Found to Improve Cancer Treatment
More recently, a study27 published in 2018 concluded the addition of baking soda can improve the effectiveness of conventional cancer treatments. According to these findings, published in the journal Cell, when tissues are acidic, cancer cells can go dormant, thereby allowing them to hide from the treatment. Lead author Chi Dang told   "Many of the therapies we have — chemotherapy, targeted therapy — work in cells that are actively functioning and dividing. When you awaken cells from a resting state into an active state, they become more vulnerable to cancer therapy."   This study also found that when pH is low, it disrupts your circadian clock. "Buffering against acidification or inhibiting lactic acid production fully rescues circadian oscillation," the researchers found.29 Acidification also suppresses mechanistic target of rapamycin complex 1 (mTORC1) signaling, and this too plays a role. According to the authors:   "Restoring mTORC1 signaling and the translation it governs rescues clock oscillation. Our findings thus reveal a model in which acid produced during the cellular metabolic response to hypoxia suppresses the circadian clock through diminished translation of clock constituents." expounds on the findings:30
"'What we've discovered in this study is that there's a very rapid mechanism by which low pH, or acid itself, turns off a key toggle in the cells that controls the cell's ability to make proteins,' Dang said. In other words, it prevents cells from dividing.  As their processes slow down, the cells go into hibernation, making them invisible to cancer treatments. Dang and his team wanted to see if they could reverse that process, and they came up with a simple solution: neutralizing the acid with baking soda.
They tested their theory by adding baking soda to the drinking water of mice that had been grafted with tumors. 'What we found is that the areas that were acidic, now are no longer acidic, and they become more active,' Dang said.   'So this toggle comes back on, so that cells that are at rest can now be reawakened.' That allows chemotherapy and other treatments to find and destroy cancer cells … "

Monday, August 26, 2019

How to Be Aware of Your Heart Attack Risk

How to increase your health span

Analysis by Dr. Joseph MercolaFact Checked


  • A primary hindrance to extended health span is the process of atherosclerosis, the hardening of your arteries, which is the No. 1 cause of heart disease
  • Your coronary artery calcium or CAC score is a powerful measure of your cardiac disease risk. Having a CAC score of zero in middle age means you have a very low risk (1.4%) of heart attack in the following decade; above 1,000, your risk of a heart attack within the next 10 years is 37%
  • While age is typically seen as the primary risk factor for CVD, the CAC score takes precedence when it comes to identifying your real risk, and transcends other risk factors
  • High LDL particle count can be a significant risk factor for CVD, but several factors also play a role, and will determine whether high particle count is contributing to atherosclerosis. These include oxidized LDL, damaged glycocalyx, endothelium damage, proteoglycan reactivity and poor HDL functionality
  • Factors that drive atherosclerosis and should be avoided or addressed include glucose spikes, insulin resistance, inflammatory drivers, high blood pressure, oxidative stress, nutrient deficiencies, iron overload, heavy metals, autoimmune issues, infections and smoking
Ivor Cummins is a biochemical engineer with a background in medical device engineering and leading teams in complex problem-solving. On his website,,1 he offers guidance on how to decode science to transform your health.
In the featured lecture, "Avoiding and Resolving Modern Chronic Disease" presented at the Low Carb Denver 2019 conference,2,3 Cummins discusses the root causes of heart disease and other chronic health problems that rob us of our health span.
His father, who died of heart disease, also suffered with vascular dementia for about 15 years. In total, Cummins believes his father lost about 20 years of his health span — years he could have had, had he had access to better information.
According to the statistics Cummins cites, about 30% of people lived past the age of 70 in 1925. Since then, our life span has improved. Nowadays, a greater percentage of people live well into their 80s and 90s, compared to 1925.
However, Cummins believes that with appropriate nutrition and lifestyle modifications, we could live well past 100, and more importantly, remain healthier far longer than we are now.
As noted by Cummins, there's little point in living longer if you're chronically ill and cannot enjoy your life. He proposes that the primary hindrance to extended health span is the process of atherosclerosis, the hardening of your arteries, which is the No. 1 cause of heart disease.
By implementing the appropriate lifestyle strategies, you can prevent or at the very least stabilize the disease progression, thereby avoiding a life-threatening heart attack.

Understanding your CAC score

In his lecture, Cummins discusses the importance of your coronary artery calcium or CAC score, which he refers to as "the master measure for cardiac disease."
As noted by the American College of Cardiology,4 a CAC scan "is one way to estimate someone's risk of developing heart disease or having a heart attack or stroke." The reason for this is because calcium deposits in your arteries signal buildup of plaque, which over time hardens and narrows your arteries.
The thicker your arteries, the higher your score. Cummins cites research5 showing that having a CAC score of zero in middle age means you have a very low risk (1.4%) of heart attack in the following decade.
A low score between 1 and 100 raises your risk to 4.1%, an intermediate score between 101 and 400 raises your risk to 15%, and a high score between 400 and 1,000 puts your risk at 26%. Above 1,000, your risk of a heart attack within the next 10 years is 37%.
He also cites data from the Framingham study showing the cardiovascular disease (CVD) risk for seniors with a zero CAC score is nearly identical to that of a 50-year-old with a zero score. Ditto for those with intermediate scores.
In other words, while age is typically seen as the primary risk factor for CVD, the CAC score takes precedence when it comes to identifying your real risk, and transcends other risk factors. Needless to say, if you stop the progression of calcification, you decrease your future risk of CVD, and the earlier you catch it, the better.
The CAC scan takes about 30 minutes and costs between $100 and $400.6 While some health insurance plans may pay for this test, most do not, so check your plan details. Ideally, discuss your need with your doctor, who can refer you to a facility that performs the scan. There are also walk-in CAC scan clinics around the U.S.,7 but you'll still need to share the results with your doctor to have him or her interpret them for you.

What drives CVD progression?

To prevent atherosclerotic progression, you need to know what the driving factors are. Cummins compares data of calcification rates in Western white men and those of indigenous cultures.
The differences are provocative, with indigenous Tsimane men having virtually no calcification even into their later years, and even though they have very similar low density protein (LDL) particle counts (a well-recognized risk factor for CVD and the focus of Cummins' lecture) as white men.
What lifestyle differences may account for these discrepancies? According to Cummins, these indigenous tribesmen have:
  • An all-natural, unprocessed diet and healthy omega-3-to-omega-6 ratios
  • Low blood glucose and insulin levels
  • No diabetes, metabolic syndrome or hyperinsulinemia syndrome
  • No hypertension
  • No central obesity

Heart healthy strategies

If you want to protect your heart and live a healthy life well into your retirement, Cummins believes the following factors are the most important. As you will see below (and in his lecture), these factors are all underlying drivers of atherosclerosis. Thus, to avoid CVD you'll want to:
Avoid glucose spikes and insulin resistance
Avoid inflammatory drivers
Maintain healthy blood pressure
Limit oxidative stress
Address mineral and vitamin deficiencies
Avoid iron overload
Avoid heavy metal exposure and/or addressing heavy metal toxicity
Address autoimmune issues
Avoid and address infections
Quit smoking

Factors that influence the effects of LDL

Cummins presents a model based on the airline industry's airplane crash trajectory. There are many defense systems in place, and a failure must appear in each system layer for a crash to occur. The same model can be applied to CVD. In order for a heart attack to occur, more often than not, multiple factors must line up.
You're probably familiar with the theory that high LDL particle count can be a significant risk factor for CVD. Cummins warns that should a dietary change cause your LDL particle count to skyrocket, you'd be wise to investigate further. To assess whether high LDL particle count is actually a problem, the following factors need to be taken into account, as they all play a role:
Oxidized LDL in your bloodstream — According to Cummins, recent research shows it's damage to the LDL in your blood that leads to oxidized LDL. Oxidized LDL is allowed into your arterial wall through the LOX-1 receptor, thereby contributing to the atherosclerotic process.
Meanwhile, undamaged LDLs "do not appear to partake in the process in a meaningful way," Cummins says. So, if you have high LDL particle count, you'll want to know whether or not they're oxidized. The list above (of strategies that will protect your heart), are things that will affect the oxidation of your LDL.
Damaged glycocalyx — The glycocalyx are tiny hair-like protrusions on the inside of your artery that act as a sieve for LDL. It regulates many of the components that determine which particles will be allowed to enter the artery wall.
The paper8 "Hypothesis: Arterial Glycocalyx Dysfunction Is the First Step in the Atherothrombotic Process" details the role of the glycocalyx. According to Cummins, scientists have identified the following factors as being damaging to the glycocalyx, which also match his list of CVD prevention strategies above:
Diets high in sugar and processed foods
High blood pressure
Oxidative stress
Oxidized LDL (but not native LDL)
Arterial morphology
Damaged endothelium — The endothelium is a single-celled layer inside your artery that manages the damaged LDLs entering the arterial wall. (In his lecture, Cummins explains the two ways in which LDL's can enter your arterial wall.)
Factors that damage your endothelium, allowing LDLs to be driven across it, include the following. Again, most of the items on Cummins' list of things to avoid to protect your heart will trigger these endothelia damaging factors:9
C-reactive protein
Oxidized LDL
Oxidant induction
Reactive oxygen species
Lipopolysaccharide ingress from infections and leaky gut syndrome that causes an immune reaction
Tumor necrosis factor
Angiotensin II
Interleukin-I 7
Proteoglycan reactivity — Proteoglycans are hair-like structures inside your arterial wall that can trap LDL particles and cause them to oxidize. What makes LDL particles get stuck here?
According to Cummins, the research shows it's not LDL particle size per se that matters most. Heart attack patients, Type 2 diabetics and those with insulin resistance all have higher proteoglycan reactivity, and Cummins believes his list (above) covers most of the issues that these people have. 
Damaged high density lipoprotein (HDL) efflux — High HDL is typically viewed as being protective, but that's not the whole story. As explained by Cummins, HDL helps remove cholesterol from your arterial wall.
As long as the HDL can keep up with the incoming cholesterol, buildup is prevented. Problems can occur, however, if your HDL become inefficient at their task. The importance and impact of HDL functionality is detailed in the paper10 "HDL Cholesterol Efflux Capacity and Incident Cardiovascular Events."
The researchers measured not just the HDL level but the actual functionality of the participants' HDL. Those with highly functional HDL had a significantly lower risk of CVD than those with poorly functioning HDL. "This is the real story on HDL," Cummins says. So, how do you lower the functionality of your HDL? Fail to address the items on Cummins heart-health list.

Ketogenic diet is part of the answer

In short, the risk factors Cummins lists (high glucose and insulin levels, inflammation, high blood pressure, oxidative stress and so on), all damage your arteries in ways that allow LDL to cause CVD. Yet for the past half-century, the medical community has been near-exclusively focused on cholesterol while largely ignoring the root causes.
Unfortunately, as noted by Cummins, the media has been complicit in creating bad press and misleading information about lifestyle strategies that can effectively address these root causes, such as nutritional ketosis. The "keto crotch" disinformation, for example, was a PR ploy designed to scare people away from the ketogenic diet. 
"All of this media has a chilling effect in applying low-carb or keto, and because a majority of our adult population are now essentially diabetic, we need low-carb and keto to fix the real root causes," Cummins says.
To extend your health span (and not just your life span), Cummins points out you need to do your due diligence as early as possible, which means addressing the root causes as early in life as possible.
cyclical ketogenic diet can go a long way toward addressing those issues, lowering inflammation, normalizing your blood glucose, insulin and blood pressure and so on. Aside from eating a low-carb diet, Cummins also recommends:
  • Eliminating industrial seed oils and processed foods from your diet
  • Eat more low-mercury fish and optimize your omega-3 index
  • Eat nutrient-dense whole foods, including eggs, butter and other healthy fats
  • Get healthy sun exposure on a regular basis (making sure not to burn)

Diagnostic recommendations

In summary, Cummins recommends getting regular lab work done to track your status. If your CVD risk based on your lab work is really low, you probably don't need a CAC scan.
If your lab work indicates high risk, you don't need a CAC scan, as you need to take action to lower your CVD risk anyway. CAC is best for those in the middle, who want to fine-tune their risk assessment.
If your CAC score is low, maintain a healthy lifestyle and retest in five to seven years to make sure you're still on track. Midrange scores are indicative that changes are needed, if you want to lower your CVD risk. If you haven't already implemented the prevention strategies listed earlier, now's the time.
If your score is high, Cummins recommends following up with expert assessment of more comprehensive blood panels — such as A1C, GGT, ferritin, homocysteine and others — to pinpoint where the problem lies.
In the case of a high score, you may want to do another scan in about two years to get an idea of what your trajectory is — are the changes you're making producing the desired results? If not, what may you be doing wrong, or what have you failed to address?
A high score also means you have little room for cheating — you'd be wise to implement as many healthy lifestyle strategies as possible, and be strict about maintaining them.
Just remember, your body has a remarkable way of self-healing, given half the chance, and as Cummins notes, we now know a whole lot more about what's required for good health than we did in decades past. The key is to implement this knowledge.