![]() Success versus Failure: A stark juxtaposition - In April I was part of a panel at the Milken Global Conference, the title of which was something like, “Keys to a healthier and more prosperous society.” The panel was moderated by Michael Milken, and it was great to meet him and his rock- star staff (especially Shawn Simmons, Paul Irving, and Nancy Ozeas). The other panel members were seasoned vets of the obesity discussion: Troy Brennan (Executive VP and Chief Medical Officer of CVS Caremark), Tom Frieden (Director of the CDC), Lynn Goldman (Dean of the School of Public Health at the Milken School of Public Health, at George Washington University), and Dean Ornish (president and founder of the Preventive Medicine Research Institute). I was the pauper in the group—no big credentials and zip- zero “panel” experience. A few weeks before panel, we all jumped on a conference call and Michael set the stage for the discussion he wanted to moderate. This is unacceptable.”Who could disagree? Hell, I usually only reference the direct cost of obesity and its related diseases—about $4. Now that is really un- effing- acceptable. ![]() ![]() So, back to the panel. The idea of being on a panel kind of freaked me out, even more than the sheer terror and vulnerability of TEDMed. The possible need to be defensive. Propane is used in a number of applications, the most common being a heating fuel. While the Houston heating season is limited, our location, size and industrial. Fundamentals of Heat and Mass Transfer 7th Edition Bergman Solutions Manual. Sound bites over substance. I don’t enjoy debates. Nothing comes of them. Just greater and greater polarization. The “winner” isn’t even necessarily the one with the best “facts.” Gary Taubes shared this quote with me recently, which I find really insightful. Dallas Willard, a well- known ecumenical pastor and theologian, was often invited to debate the existence of God and other matters. These invitations included Richard Dawkins himself. We will seek the truth together.” That’s the attitude I like. In the end, I decided to just tell a few (in some cases provocative) stories. Because it’s easy to present reams of data, yet so few people remember the point. You don’t need to care one iota about training cardiac surgeons to realize the gems in this piece.)I realized going into this that I would be the contrarian in the group.
I don’t claim to know all (or even many) of the answers, but I’m willing to bend over backwards in search of them. I realize folks (from readers of blogs to members of the audience at the Milken Global Conference) want facts, answers, prescriptions. I think we need to know more, first. Below are the notes I made for myself in the days leading up to the panel. Basically, I wanted to tell a few stories, plus summarize it all (if given the chance). ![]() I didn’t actually “practice” this or even take notes up on stage (which I regretted when I realized everyone else was smart enough to bring notes), so if you decide to watch the actual video of the panel, you’ll note that I only vaguely followed what’s written below. I did send the video to two of the best speakers I know to get their feedback. Their feedback: could have been much better, but not the worst job ever. Lots of work to do for next time. Duly noted.)How did I find myself interested in this problem? My arrival at this place is really a coming together of two revelations. First, during my surgical residency at Johns Hopkins, not surprisingly, I was often dealing with the complications from diabetes and obesity in my patients. It slowly became obvious that all I was doing was slapping on the surgical equivalent of Band- Aids without ever addressing the underlying problem. I was treating symptoms and not the actual disease. When I would amputate the leg of a diabetic patient, which I had to do, regrettably, all too often, I knew that my patient was more than likely to be dead within five years anyway. The second revelation was five years ago—September 8, 2. I remember it so clearly. My sport of choice was marathon swimming, and I followed what I believed to be the iconic healthy athlete’s diet. I had just completed an especially difficult swim into the current from Los Angeles to Catalina Island, becoming one of a dozen people to do that swim in both directions. But you need to work on being a bit less not thin.”And not only was I, well, fat, despite all this maniacal exercise, but it turns out I was also pre- diabetic. Her comment launched me into a series of nutritional self- experiments. I was already working out three to four hours a day, so the problem couldn’t be sedentary behavior. It had to be what I ate. Over the next year I manipulated my diet until I found what worked for me, which paradoxically didn’t involve eating less, just eating very different from the food pyramid. Along the way I became obsessed with reading the nutrition literature. What I learned was that the evidence supporting our dietary guidelines was ambiguous, at best, and occasionally contradictory. There was a real dearth of evidence to support what seemed like the obvious questions. I realized then, that if the guidelines didn’t work for me and if I can’t figure this out, with my background as a doctor and someone who studies healthcare, maybe they don’t work for a lot of people. Maybe there are systemic problems here. Maybe these problems were at the root of the ongoing epidemics of obesity and diabetes. And if the studies don’t exist to give us unambiguous evidence, then raising the funds and enlisting the researchers necessary to do those studies. What does success in public health look like? When trying to understand complex problems, I like to start with success stories, identify patterns and work backwards—reverse engineering success. Consider the following graph. Research About Weight Loss Programs in Los Angeles County Associations & Licensing for Weight Loss Programs in Los Angeles County. CDA California Dietetic Association. Four CA Regional Agritourism Summits in February & March. The University of California Small Farm Program and UC Cooperative Extension advisors in four California. ![]() ![]() It shows the death rate from AIDS in the United States between 1. The point of this graph isn’t subtle. Death from AIDS rose steadily and monotonically through the mid- 9. Though people still die from AIDS, this still represents a success story in health policy and science. For those experiencing the personal tragedy of AIDS, this is salvation. So why did it happen? Well, first, the cause of the disease was correctly identified—the HIV virus—in the mid- 8. HAART therapy, was able to effectively treat the virus and prevent progression to AIDS. Again, two things happened: the cause of the disease was correctly identified, and an effective treatment was developed by an enlightened healthcare profession. This is what success looks like. The case study of “failure”Let’s take a look at this figure. It shows the prevalence of diabetes in the United States over the last hundred- plus years. As you can see, diabetes was exceedingly rare in the 1. By 1. 97. 0, around the time I was born, that number was up to 2,0. Worse yet, type 2 diabetes is now spreading into demographics previously na. I don’t think any of us in this room today would argue that we have this situation under control. So where are we failing? Many of you understand the world of business. If this were a business, we’d be asking a lot of questions at this point, or we would be out of business. Like any business, we have two possibilities. We either look at our business plan (the basic premise for how we’re going to succeed) or the implementation of that plan (the way we operate on a day- to- day basis). In other words, we don’t have the right business plan. In this latter scenario, the failure is not one of personal responsibility, but of our assumptions about the cause of this disease. And these two scenarios have very different implications. I am not certain which of these is more likely correct, but I do know the risk of ignoring the latter in favor of the former is not a choice we can make any more as a society. So, maybe the question we should be asking is whether we are right about the environmental triggers of this disease—the underlying cause. Is it as simple as gluttony and sloth and a food industry that overwhelms us with highly- palatable, energy- dense foods, or is there something specific about the quality of the food we’re consuming that triggers these disorders? If we don’t answer this question about what is it in our environment that’s causing this disease correctly, just like we were able to answer it in the mid- 8. HIV’s role in AIDS, we can’t effectively treat the disease. Instead we’re stuck putting on Band- Aids. Here’s another way to think about it: imagine this panel was on a new crisis in aviation. Planes are constantly crashing—falling out of the sky—and killing 4,0. Americans a day.) And you’re a pilot and you tell me that surely we understand the principles of flight. Sure, we might suspect user error to be part of the problem. I’m not confident that that’s the solution. Nor should you be. Is there a policy- based solution to this problem? Surely policy changes will play a necessary role in restoring our health. But it may be less about . People in this room contributed to that success. The little colored triangles on the grey line are major milestones in science (red), market forces (green), and policy (blue). This is a great example of what one might call the “critical confluence”—scientific elucidation, policy action, market response, and behavioral shift—all coming together to save lives. But, as in all things in life, algebra included, the order of events matters! Which came first then? In the case of smoking and lung cancer, it was unambiguous scientific clarity, which in this case happened in the 1. Surgeon General’s report. This information was absolutely necessary to drive the policy action, the market response, and the behavioral shift that followed. Without the knowledge that lung cancer is caused by smoking, no amount of policy or market response would have led to the necessary behavioral shift and so a meaningful reduction in lung cancer incidence. When we consider the current situation with obesity and diabetes, we may still be missing the equivalent of the scientific clarity linking unambiguously the environmental trigger (smoking) that provided the obvious method of prevention (smoking cessation). Think skinny people don’t get type 2 diabetes? Think again. i. Stock. In the last article we discussed the complex relationship between body weight and type 2 diabetes (T2. DM). We learned that although obesity is strongly associated with T2. DM, a subset of “metabolically healthy obese” (MHO) people have normal blood sugar and insulin sensitivity and don’t ever develop diabetes. In this article we’re going to talk about the mirror reflection of the MHO: the “metabolically unhealthy nonobese” (MUN). These are lean people with either full- fledged type 2 diabetes or some metabolic dysfunction, such as insulin resistance. You might even be surprised to learn that skinny people can and do get T2. DM. They are rarely mentioned in the media, and there isn’t much written about them in the scientific literature. Perhaps these folks have been overlooked because type 2 diabetes has been historically viewed as a disease of gluttony and sloth, a self- inflicted outcome of eating too much and not and not exercising enough. But the very existence of the MUN phenotype proves that there’s more to T2. DM than overeating and a sedentary lifestyle. Remember that one in three type 2 diabetics are undiagnosed. It’s possible that a significant number of these people that are lean. They don’t suspect they might have T2. DM because they’re under the impression that it’s not a condition that affects thin people. This is one of the biggest dangers of the myth that “only fat people get diabetes”. It’s well- known that high blood sugar can precede the development of T2. DM for as long as ten years. It is during this time that many of the complications associated with diabetes – nerve damage, retinal changes, and early signs of kidney deterioration – begin to develop. This is why it’s just as important for lean people to maintain healthy blood sugar as it is for the overweight and obese. It’s also important to understand that diabetes is not a disease. Every single person with T2. DM, whether they are rail thin or morbidly obese, shares a single symptom: high blood sugar. Therefore, anything that interferes with the body’s regulation of blood sugar levels will cause type 2 diabetes. What causes high blood sugar and T2. DM in lean people? Not surprisingly, the causes of T2. DM in lean people are similar to the causes of T2. DM in the obese. They can be loosely grouped into the following categories: Genetics. Fatty liver. Inflammation. Autoimmunity. Stress. Let’s discuss each of them in turn. Genetics. Studies of the lean, otherwise healthy offspring of type 2 diabetics has revealed that they are much more likely to be insulin resistant than the lean offspring of non- diabetics. One explanation for this is an inherited defect that causes mitochondrial dysfunction. People with this defect are not able to burn glucose or fatty acids efficiently, which causes lipotoxicity and an accumulation of fat inside of muscle cells. I will discuss the contribution of genetics in more detail in the next article. What I want you to understand here is that the genetic mechanisms I described above are capable of causing insulin resistance and high blood sugar independently of overweight or obesity. Fatty liver. Studies of lean, Asian Indian men have found that they have a 3- to 4- fold higher incidence of insulin resistance than their caucasian counterparts. They also have a much higher prevalence of non- alcoholic fatty liver disease (NAFLD) and hepatic (liver) insulin resistance. NAFLD is an independent predictor of type 2 diabetes. Cross- sectional studies have shown that fatty liver and metabolic abnormalities occur together. It has also been proposed that fatty liver is not just a result, but also a cause of insulin resistance and type 2 diabetes. Now, keep in mind that these Asian Indian men with NAFLD were not overweight. They were lean, and in some cases, even underweight. This proves that NAFLD occurs in lean people, and together with the evidence above, suggests that NAFLD may be a primary cause of insulin resistance and T2. DM in lean people. If you’re thinking NAFLD might be a rare problem confined to Asian Indian men, you should know that up to 3. This is a disturbingly high prevalence of a condition that is known to progress to severe liver inflammation and cancer in a small percentage of people – in addition to contributing to T2. DM and metabolic syndrome. While there may be a genetic component that predisposes people to developing NAFLD, we also know that dietary factors play a significant role. Rodent studies have shown that feeding large amounts of sugar and industrial seed oils (like corn, safflower, sunflower, etc.) promote NAFLD, whereas saturated fats such as butter and coconut oil do not. And in human infants, tube- feeding with industrial seed oils causes severe liver damage, whereas the same amount of fat from fish oil does not. Fructose, especially the high- fructose corn syrup (HFCS) found in sodas, candy and several packaged and refined foods, is perhaps the most significant dietary cause of NAFLD. The liver processes fructose by converting it to fat. The more fructose consumed, the more fatty the liver becomes. Feeding rodents high amounts of fructose promotes NAFLD, and the consumption of soft drinks (by humans) can increase the prevalence of NAFLD independently of metabolic syndrome. Let me say that again: high fructose intake can cause fatty liver disease independently of overweight, obesity or type 2 diabetes. Do you think that might be a problem in a country where soft drinks account for nearly 1. Since fructose is handled by the liver in the same way the liver handles alcohol, excess fructose produces a similar range of problems as alcohol abuse: hypertension, high triglycerides and low HDL, obesity, cirrhosis and insulin resistance. Inflammation. In the study of lean Asian Indian men above with T2. DM, it was found that they had a 2- fold increase in plasma levels of the inflammatory protein IL- 6 when compared to lean subjects without T2. DM. In a previous article I showed that chronic, low- grade inflammation associated is an important mechanism in decreasing insulin signaling and causing insulin resistance in muscle, liver and fat cells. Also, inflammation has been shown to precede the development of diabetes. Infusion of inflammatory cytokines into healthy, normal weight mice causes insulin resistance, and people with other chronic inflammatory conditions are at higher risk of developing T2. DM. For example, about one- third of chronic Hepatitis C patients develop T2. DM, and those with rheumatoid arthritis are also at higher risk. Autoimmunity. Up until recently, type 1 and type 2 diabetes were seen as distinct entities. It was understood that type 1 diabetes (or insulin- dependent diabetes) was caused by autoimmune destruction of the beta cells of the pancreas, leading to decreased insulin production, whereas type 2 diabetes was caused by insulin resistance of the liver, muscle and fat cells. However, recent research has demonstrated that the line separating these two conditions may be much blurrier than previously thought. It is now known that type 1 diabetes, which normally begins in childhood, may slowly develop later in life. This form is referred to as latent autoimmune diabetes (LADA) or more informally as type 1. Studies suggest that type 1 diabetes in adults is frequently misdiagnosed as T2. DM, and up to 1. 0% of adults with T2. DM may actually have the autoimmune form. Even more relevant to this article is the finding that fully 1 in 4 lean people with T2. DM produce antibodies to GAD, the same enzyme in the pancreas that is attacked in type 1 autoimmune diabetes. These findings suggest that a significant number of lean people with T2. DM may be suffering from autoimmune diabetes. This will obviously require a different treatment strategy than those who have the non- autoimmune form. It’s a fairly standard blood test and is available through Labcorp and Quest.)(Interestingly enough, approximately 5% of patients with autoimmune thyroid conditions also produce antibodies to GAD. So if you have Hashimoto’s or Graves’ disease along with blood sugar symptoms that don’t respond to dietary changes, you should have your GAD antibodies checked.)Stress. Under conditions of stress, the body produces higher levels of the hormone cortisol. Cortisol plays a number of important roles, but one of it’s primary functions is to raise blood sugar. This is an incredibly helpful evolutionary mechanism that is part of the “fight or flight” response that prepares us to deal with a challenge or threat. However, that mechanism was only designed for short bursts of stress. Chronic stress as we experience it today – like worrying about getting audited by the IRS, driving in traffic, and suffering from degenerative disease – wasn’t part of our early ancestors’ lives. This means that our bodies aren’t prepared to deal with the effects of chronic stress, which include chronically elevated levels of cortisol. Why? Because cortisol is capable of raising blood sugar to unhealthy levels even when a person is fasting. What that also means is that you can be lean, eat a perfect diet, and still have high blood sugar (and thus T2. DM) if you suffer from chronic stress. I’ll be writing more about the connection between stress and diabetes in a future article. Like what you’ve read? Sign up for FREE updates delivered to your inbox. I hate spam too. Your email is safe with me. Laura Hillenbrand: Guestbook. It is my desire to pass along to Ms. Hellenbrand my most sincere thanks and appreciation for her excellent work in the writing of Unbroken. Hillenbrand may have another opportunity to consider an equally impressive and remarkable story of the life of Bruce Olson. Hillenbrand to consider such a project. Sincerely,Carl R. Johnson. Brief Bio of Bruce Olson: Bruce Olson (b. November 1. 0, 1. Scandinavian American Christian missionary who is best known for his pioneering work in bringing Christianity to the Motilone Indians of Colombia and Venezuela. His story is told in his autobiographies Bruchko and Bruchko and the Motilone Miracle. Early life. Bruce Olson was born in 1. Saint Paul, Minnesota, the younger of two sons of Marcus and Inga Olson. His father was an investment banker, and his mother was a socialite. Gifted in languages, at an early age Olson learned Greek and Latin. When Olson was 1. Christian conversion, the experience of being born again, while reading the New Testament. He had seen God as a stern, judgmental figure, and became very critical of Lutheran churches. Then in Luke 1. 9: 1. Olson encountered another depiction of God: “For the Son of man is come to seek and to save that which was lost.” Olson had known that he was lost – separated from God by his sins. But here he discovered that God wanted to find him. That night, Bruce Olson spoke to Jesus, and asked Jesus to satisfy him with the same peace and fulfillment that he had read about in the lives of Jesus’ apostles. He asked Jesus to help him be a person who pleases God. From that moment on, Olson’s life was changed. At the age of 1. 6, Olson attended his first missionary conference, at the church he began to attend after his conversion. The missionary speaker, a Mr. Rayburn, spoke of his work with the people of New Guinea. Rayburn challenged the congregation to realize that people around the world were starving and dying, separated from Jesus by their sins. Rayburn challenged them to not only put money in the collection plate to help these people, but to go themselves. At that moment, Olson knew that God wanted him to become a missionary to the Indians of South America. In the fall of 1. Olson enrolled in Penn State, transferring to the University of Minnesota a year later to study linguistics. In the meantime, Olson applied to several missions boards, but was rejected as a missionary candidate. But in early 1. 96. Olson left college, bought a plane ticket to Venezuela. At the time, he spoke no Spanish, and had only a few dollars in his hand. Shortly after arriving in Venezuela, Olson heard about the Motilones, a violent stone- age tribe living on the borders of Venezuela and Colombia that had been in the news because of violent clashes with oil company employees, seeking to drill on their land. No one in the outside world knew anything about Motilone culture, their language or their life. Olson felt a strong pull towards making contact with the Motilones. Work with the Bar. They believed in the existence of a single God, and that evil spirits existed in the world. But they believed that God had rejected them for deceiving Him. A man named Sacamaydodji had come to them, claiming to be a prophet, saying that he could take them over the horizon to a better land. They left God and followed him, but eventually came to believe that Sacamaydodji had been a false prophet, and regretted walking away from God. Still, they had a prophecy that a tall man with yellow hair would come with a banana stalk, and that God would come out of the banana stalk. With much difficulty, and after being shot with Motilone arrows, Olson began to live with the Motilone in 1. For one thing, he discovered that the name “Motilone” was a Spanish name for the tribe, meaning “people of short hair.” The Motilone call themselves “Bar. As he grew more and more familiar with the tribe,Olsen got the nickname Bruchko given to him by the Motilone. He began to see ways he could help them. Olson began his work by befriending the tribe’s medicine woman. Olson realized that for him to bring cures to the people would undermine the traditional authority structure in their culture. During an epidemic of pink eye, he watched the medicine woman chanting over the afflicted, asking God to heal them. Olson asked her about the cure, and she sighed, saying that she chanted, but God would not help them, since they had deceived God. Olson went out of the house, and asked an old man afflicted with pink eye if he could touch the corners of his eyes. The old man agreed, and Olson smeared some of the old man’s infected tears into his own eyes. Olson quickly developed pink eye himself, and went to the medicine woman for help. She chanted over him, but the pink eye was not cured. Olson gave her some antibiotic ointment, and asked her to apply the ointment to his eyes while she chanted a new chant – perhaps because he was an outsider, the old chant didn’t work on him. Within a few days, the pink eye had cleared up. The medicine woman tried the new chant on others of the afflicted, with no results. Then she asked Olson for his “potion,” and sure enough, when she applied the antibiotic and the chant, the pink eye was eradicated. Her success elevated her status in the eyes of the tribe, and cemented Olson’s bond with her. Within the tribe, Olson formed a pact with a young man named Bobarishora, becoming adoptive brothers together. The two worked together, visiting many Bar. One day in 1. 96. Olson’s pact- brother Bobarishora cut open a banana stalk, and the leaves inside splayed out, like the pages of a book. Olson pointed to his Bible and said, “This is God’s banana stalk!” Olson recounted a Bar. Miraculously, the man was transformed into an ant, and as an ant, he was able to show the other ants how to improve their home. Olson used that story to describe how God became incarnate in Jesus, and “walked our trail.” Olson described the death of Jesus, and his resurrection, and told the Bar. Olson had difficulty explaining “faith” in the Bar. Olson reminded Bobarishora of one of his first celebrations with the tribe, when he was afraid to climb into one of the high- strung hammocks loved by the Bar. He had wanted to keep one foot on the ground, but Bobarishora had told him that he could only sing if he was fully suspended in the hammock. Olson said, “That is how it is when you follow Jesus, Bobby (Bobarishora). No man can tell you how to walk His trail. But to find out you have to tie your hammock strings into Him and be suspended in God.” Two days later, Bobarishora told Olson, “Bruchko, I’ve tied my hammock strings into Jesus. Now I speak a new language.” For the Bar. Bobarishora spoke of having a new life, suspended in Jesus. Months later, at the tribe’s Festival of the Arrows, a time of pact- making and story- telling, Bobarishora was challenged to a singing competition by an older chief named Adjibacbayra. Climbing into a single hammock, the two men sang alternating lines, and Bobarishora sang about how the Bar. The song lasted over ten hours, but the effect was startling. The entire tribe accepted the song about Jesus. Soon, the song had spread to other Bar. Within months, virtually the entire Bar. He lives in the jungle on the border of Colombia and Venezuela.
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