For that reason, when doctors couldn’t find the primary source of his cancer, my dad insisted he must have colon cancer. After numerous diagnostic tests, including CAT scans, X-rays, and colonoscopies, my dad went in for yet another colonoscopy, taxing his already weak body to receive yet another confirmation that he did not have colon cancer. He had valiantly shrugged off last year’s cancer diagnosis for seven months but now the symptoms were too conspicuous—and quite frankly, too acute—to ignore. So he decided what type of cancer he had.

From the secrecy he obstinately maintained surrounding the cancer to distrust of the oncologist and gastroenterologist bearing bad news to poor choices made about treatment, my dad’s battle with cancer was froth with lessons learnt after the fact. The unfortunate thing is that I quickly found out his experience is not uncommon amongst immigrant populations. This Cornell graduate, an engineer who had lived in the States for over four decades still had a “back home” cultural lens through which he approached sickness.

At a trip to his bank, a banker I’d just met commiserated with me because her mother had worn those lenses as well. “Somebody needs to educate them,” she said.

Last week a paper was published in Nature’s American Journal of Enterology, heralding increased rates of colonoscopy screening in New York City for all ethnicities over 50,  an increase that closed an almost 30-year long racial and gender gap. This is undoubtedly a major accomplishment for the Columbia Mailman School of Public Health, the New York City Department of Health and Mental Hygiene, and the Citywide Colon Cancer Coalition, who together spearheaded a five-year long multifaceted campaign throughout the city. The campaign included media ads and outreach to the medical community. Does more screening mean less colon-cancer-related deaths? That remains to be determined, but more screening does mean that a concerted multifaceted campaign can effectively reach all New Yorkers, not just those who are U.S-born, college-educated, 65 and over, and living at twice the federal level—the ones who had the highest rates of increase in screening. Indeed, a lot is to be learned from the campaign’s success.

New York is an urban city, a hub of all nations, home to the United Nations headquarters; it makes me shudder to realize that our immigrants were not targeted more effectively in this multifaceted campaign. The barriers to health that are unique to immigrants are being painstakingly penetrated by grassroots organizations but perhaps there would be a greater magnitude of contact if the city and major universities teamed up with these organizations to change the health outcomes of immigrants.

Source: epochtimes.com

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The epidemic of obesity in America has hit every ethnic group in America, and African American women have soared to the top with an almost 50% incidence rate by 2008, as reported by CDC. The prevalence of type 2 (T2) diabetes, or adult-onset diabetes, is also on the rise. While physical inactivity and obesity have been shown to be leading risk factors for T2 diabetes, the biological mechanism behind this association has been elusive. Last week Dr. Tapan Chatterjee and his team of cardiac researchers at the University of Cincinnati announced the discovery of a new pathway that may provide the missing link to obesity and T2 diabetes.

One characteristic of obesity is dysfunctional fat cells. In obese people, precursor fat cells fail to differentiate into fully functional fat cells that are able to store excess calories. This phenomenon has also been shown to associate with type 2 (T2) diabetes, insulin resistance and heart disease. Researchers found a pathway that is critical in differentiation of fat cells. And at the center of this pathway is the enzyme histone deacytelase 9 (HDAC9).

Chatterjee reported that mice lacking HDAC9 had accelerated differentiation, while those with increased levels of HDAC9 had low amounts of differentiated fat cells. In addition, mice that were chronically overfed had high levels of HDAC9. These mice had dysfunctional fat tissue and low production of proteins necessary for maintaining lipid and glucose stability. Here, we see HDAC9 linked to defective fat cells (like in obesity) and poor glucose uptake (like in T2 diabetes).

People with T2 diabetes produce not only inadequate amounts of insulin but also ineffective insulin that does not enable glucose to be taken up into skeletal muscle. This leaves high levels of glucose in the blood, which is the glucose instability characteristic of T2 diabetes.

Whether HDAC9 levels cause or contribute to T2 diabetes in obese people remains unknown. Nevertheless, Chatterjee’s team is doing studies to determine if targeting HDAC9 in chronically over-fed mice can protect the animals from the accumulation of dysfunctional fat cells and its associated disorders. This could be the key to treating T2 diabetes in obese people.

But it may not be the only key. HDAC9 and other histone deacytelases similar in structure prevent one of the first steps in the process of generating necessary body proteins from DNA; therefore it is possible that other histone deacytelases may be involved in the pathway as well. Interestingly, HDAC9 and HDAC5 have been shown to be necessary for repressing cardiac muscle growth. Also, since HDAC9 plays important roles in different processes, targeting the gene would not disrupt fat cell differentiation only. Indeed further studies have to be done to identify other genes involved in this pathway.

What an atrocity! We can agree on that now, but the scientists’ commitment to research, to determining if penicillin can be used not just as a cure but as prophylaxis, that is, prevention, is undeniable.  The most straightforward way to explore this question was by treating patients immediately after they got infected with the syphilis-causing bacteria. And the most straightforward way to control when patients got infected was by infecting otherwise healthy people.  So, though approximately 1500 Guatemalans were given the bacteria, these victims were treated with penicillin (unlike in the Tuskeegee syphilis study which took place in the South for forty years, ending in 1972).  Indeed, this study had a noble motive with careful methodology, but the result was still unethical behavior. Why?

The underlying reason is that this research was clearly informed by prejudice–prejudice against the populations that were infected. Dr. Reverby of Wellesley College, in the tell-all paper that unearthed this embarrassing skeleton, reported that researchers thought syphilis was more frequent and aggressive in Latins than in Indians. This was not scientific fact, but rather a prejudice rampant in  U.S. society that was co-opted by the scientific community. Indeed, the 40′s was wrought with sexism, racism, and elitism, and unfortunately, science was not immune to these -isms.  In the case of this syphilis study, we see that though the research was done on confined people,  science itself was confined, chained to culture and it’s unjust biases.

Has modern-day science rid itself of these chains? Well, to some degree.

Take for example, on Monday of this week when NIH scientists published a paper in the Journal of American Medical Association, stating, “The 1946-1948 inoculation study should never have happened, and nothing like it should ever happen again.”  The paper outlined ethical violations in the form of a breach of informed consent, deception, and intentional infection; it also outlined ethical codes that have been established for the international scientific community. Indeed these are steps to remove science’s bondage to culture.

But the chains still hang. In a recent post, I noted that just two months ago, the first microanalysis of African TB patients was published; it is one amongst many already done on European TB patients. Why did it take so long for such research to be done on a people group with such high  rates of TB?

I suggest our hearts not only burn against the injustice done to the confined Guatemalans, but also regrettably  recognize that science too was also confined, restricted by cultural biases. In some ways, the victim became the victimizer.

In the words of songstress, Asa:

This movie, in all it delicious ostentatious “uber-dramaticity,” was bursting with painful reality. And a study published a few weeks ago in The Lancet confirmed it: cancer is a leading cause of death in the developing world. Scratch out all notions that cancer is a disease of the rich; these countries have 80% of the cancer deaths in the world but receive only 5% of the global resources for cancer. One can only imagine the cyclical nature of these findings; with little financial and professional resources, cancer deaths can increase rapidly.

Researchers from different parts of the world, including third-world countries, called for increased advocacy and education to raise both global awareness of this issue and more investment of international funds. However, what often starts off as well-intentioned philanthropy can often become a crutch, as those receiving aid become completely dependent on those giving aid, thereby remaining helpless victims. Perhaps in an effort to tackle this, the paper impressively highlighted case studies in Haiti, Malawi, and Rawanda, where skilled international professionals trained local community health workers—usually unskilled— to administer treatment. This impartation of knowledge I believe is key to empowering a people group and limiting the “helpless victim” phenomenon.

The prevalence of cancer in developing and developed countries points to the globalization of disease, making the world seem even smaller. Disease, like everything else, is never isolated.

In the past, lipoinjection of fat cells only, without stem cells, were used for breast enlargement, but fat cells would unpredictably die – a probably devastating loss for breast cancer patients who’d already experienced the ablation of a part of themselves when cancerous lumps were first removed. By harnessing stem cells which induce blood flow, the fat cells are able to stay alive by essentially feeding off the blood like vampires! The tissue can also regenerate! (Because stem cells keep promoting growth, do the fat cells have a greater chance of becoming cancerous? Excellent question; stay tuned)

A four year study ending in 2007 included breast cancer patients; I can’t find any published findings. Only one clinical study is reported that tests this procedure for merely cosmetic augmentation; while results were positive for the 40  Japanese participants, the time period studied was only 2 months after the operation.

Data seems far from conclusive, yet others have jumped on the bandwagon:  namely, the everyday British woman desiring to improve her figure. Times Online reports a study is being done in Britian with healthy women. If the procedure should prove to be safe and effective, the cost for this cosmetic surgery is predicted to be the equivalent of $9500.

My guess is that the technique will soon make its way to the U.S. market and sell like hot cakes. Should wealthy minorities partake while the majority of their counterparts struggle to afford treatment for serious medical conditions?

We’ve all heard the moral dilemma, which the NIH dealt with by only funding research using embryos discarded after in vitro fertilization. Under this regulation, no embryos were created specifically to be destroyed for stem cell research, although one could begin to question the ethics behind the creation of many embryos during in vitro fertilization—where only one will be used— for the purposes of fulfilling one’s desire to have an offspring. Seems like a far less noble reason to “discard” life when compared to the possibility embryonic stem cells present: of treating human diseases that affect millions of people worldwide. The battles we choose to fight in the name of religious morality! So people remain skeptical.

One reason for skepticism as mentioned in the New York Times is the therapeutic use of adult stem cells. Last week, the first U.S. trial treating stroke patients with their own stem cells, derived from the bone marrow, began! Exciting, indeed! Unlike embryonic stem cells (ESCs), which are totipotent, adult stem cells are pluripotent and can transform into many, but not all, kinds of tissue. This is limitation #1 of adult stem cell therapy. In this trial, stem cells are harvested from the leg and put in the arm, where they cross the barrier that protects the brain from invading molecules and settle in the brain to promote blood flow. Limitation #2: the route to the site of injury. What prevents the stem cells from nestling elsewhere? Still, folks are skeptical of ESC research.

Instead, what about using induced pluripotent stem cells (iPSCs)? That is, somatic cells of any type from the body that can be extracted, grown in a dish, treated with some factors and voila! They become transformed into ESCs. Again, they are pluripotent and not totipotent. Furthermore, it just so happens that the factors given to these cells are also cancer-promoting (like cMyc and Oct4 proteins). IPSCs have the potential to undergo genetic reprogramming after time, generating cancerous cells.

While all these alternatives to embryonic stem cell research are promising and worthy of further study, they do not upstage ESCs. And thanks to NIH regulation, religious folks, namely Christians, do not have to feel pigeonholed into vehemently opposing ESCs. Let the skepticism go!

Treatment is mainly a cocktail of antibiotics, but with  multidrug-resistant strains looming, the phrase “prevention is better than a cure” takes on even more gravity. To make matters worse, the world’s only prophylactic treatment of TB, the Bacille-Calmette Guerin (BCG) vaccine, is not recommended; it is ineffective in adults and provides limited protection for children. A new study may put BCG on the map again. Researchers at the University of Texas Health Science Center have discovered a way to improve its efficacy: simultaneously treat patients with a drug that induces the breakdown of certain compartments within their own cells!

The process is called autophagy, when a region of the cell becomes surrounded by a membrane, fuses with a cell component called the lysosome, and becomes degraded, leaving behind refuse that immune cells recognize as a foreign particle called an antigen. That “refuse” is integral to generating an immune response against future run-ins with the antigen.

This new technique is successful because BCG, a weakened form of the bacterium that causes TB in cattle, hides within cells so it is not recognized by the immune system. Coupling BCG vaccination with rapomycin-induced autophagy in mice exposes BCG; in this study, it led to enhanced detection of one BCG antigen, localization of BCG to lysosomes, and immune response against TB! Score!

Undoubtedly, early detection is key to successfully treating the disease. But according to research  presented at the Conference on the Science of Cancer Health Disparities in Carefree, Arizona on Tuesday, minority women are still lagging in the rates of screening for cancer, sometimes due to medical distrust.

A study at the Michigan State University showed that nearly half of the 341 Arizona, Latina, Arab, and African-American female participants believe that health care organizations deceive patients. Almost two-thirds (64 percent) of the women who had not received a clinical breast exam in the past year doubted the ability of their health care provider.

Lead author and MSU professor of obstetrics, gynecology and reproductive biology, Karen Williams, points out that since medical distrust spans ethnic lines, the forty-year-long Tuskegee Study of Untreated Syphilis in the Negro male cannot be the source of such doubt.

“Intellectuals in medicine like to link all issues of mistrust to that study because it lets us off the hook for anything that might be happening today,” said Williams. “This study shows that even groups without that history are showing a level of mistrust, so the problems must be more systemic than that.”

So what could account for the lack of trust in your friendly doctor? I propose it could be an underlying sense that the medical community generally devalues the lives of minorities. Perhaps it could be lack of recruitment of minorities to clinical trials, or the lackadaisical approach to health care that minorities have experienced when trying to obtain treatment. (Maybe the crux of the problem is the love of money over human lives, as capitalism often seems to drive health care.) I hate generalizing and would love to be corrected if my suspicions are wrong. Maybe a study will be done to objectively quantify reasons for medical mistrust…

In order to put a stop to this, risk factors must be identified and effectively reduced. A recent study in the Journal of Clinical Investigation zooms in on obesity-related childhood liver disease, showing that maternal diet high in fat, not maternal obesity, may be the culprit here.

In the study, female monkeys fed a high calorie, high fat diet (like the typical American diet) during early fetal development of their children had offspring displaying signs of liver disease as well as increased body fat. When the diet was switched to a low fat one during a subsequent pregnancy four years later, the symptoms in the offspring decreased regardless of the mother’s weight. The implications of the study are obvious, but future research needs to be done to confirm any link between maternal diet and fetal programming that contributes to susceptibility to disease.

So expecting mommies, just think about your unborn baby the next time you hanker for some greasy General-Tso’s chicken.

Reference

McCurdy CE, Bishop JM, Williams SM, Grayson BE, Smith MS, Friedman JE, Grove KL.Maternal high-fat diet triggers lipotoxicity in the fetal livers of nonhuman primates. J Clin Invest. 2009 Jan 19. pii: 32661. doi: 10.1172/JCI32661. [Epub ahead of print]