A couple of the medical news items that surfaced in the past few weeks are decidedly positive, so I will put those at the end of this installment in the hopes of preparing you for the new year in a cheerful state of mind. But I want to emphasize a point about information that – at first glance, at least – appears to be negative. Specifically, that in the context of healthcare, often it’s better to get bad news than no news at all. The bad news at least can point to a treatment pathway, but ignoring or being unaware of a potentially harmful condition in our bodies can lead to seriously negative outcomes.
Consider prostate cancer. It is the second leading cause of cancer death in men; more than 35,000 prostate cancer deaths are expected this year in the US. When prostate cancer is diagnosed in the early stages, the five-year survival rate is over 99%, but when the cancer advances to the later stages, that survival rate drops to 37%. Therefore early detection can be a life or death matter.
Prostate cancer is usually detected by means of a blood test to determine levels of prostate-specific antigen (PSA), which is a protein enzyme produced primarily by cells in the prostate gland. In healthy men, small amounts of PSA naturally leak into the bloodstream, which is why it can be measured through a simple blood test. PSA levels normally increase with age. In men up to 49 years of age, PSA levels up to 2.5 milligrams per milliliter are considered a normal range, but in men 70 to 79 years of age PSA levels up to 6.5 mg/ml are considered normal. However, many healthcare professionals use 4.0 mg/ml as the upper limit of normal. The PSA test was routinely done as part of an annual physical. This was the recommendation of many medical societies.
The U. S. Preventive Services Task Force (USPSTF), has diverged from that position for more than 20 years. Its official-sounding name notwithstanding, the USPSTF is not a government agency. It is an independent panel of volunteers with knowledge of primary care and prevention that issues recommendations for clinical preventive services. In 2012, the USPSTF guidelines gave a “D” grade to PSA-based prostate cancer screening stating “the benefits of PSA-based screening for prostate cancer do not outweigh the harms”.
A 2018 article in the Journal of Clinical Oncology (36, 37, 2018) observed that the rate of screening declined substantially from the pre-guideline period to the post-guideline period, from a rate of 42.7% of eligible men screened per year during 2010/2011 to a rate of 32.5% of eligible men screened per year during 2014/2015. In those same time periods, the rates of prostate biopsy and overall prostate cancer detection declined even more sharply. That article concluded that following the 2012 USPSTF statement, significant declines in PSA testing, prostate biopsy and overall cancer detection rates were seen along with a significant increase in the rate of patients presenting with metastatic disease.
We cannot specifically conclude that the declines in prostate biopsy and cancer detection were what led to the significant increase in metastatic cancer, but it certainly seems likely. If the cancer is not detected at an early stage, it will probably grow and metastasize.
In 2018, the USPSTF released a final recommendation statement on screening for prostate cancer, as follows: “Based on a review of the evidence, it is recommended that men aged 55 to 69 years make an individual decision about whether to be screened after a conversation with their clinician about the potential benefits and harms. For men 70 years and older, the potential benefits do not outweigh the expected harms, and these men should not be routinely screened for prostate cancer.”
What are the “expected harms” associated with prostate cancer screening? Routine prostate cancer screening, by the way, is simple and cheap – a simple blood test does the trick. If the PSA is found to be at dangerous levels, a biopsy is necessary, but a biopsy is way better than letting a localized cancer metastasize. Biopsies of the prostate are relatively quick and require only local anaesthetic.
The “expected harms” noted by the USPSTF include anxiety about the possible results. The USPSTF’s recommendation that men 70 years or older should not be routinely screened is based on their assumption that these men will not live long enough to be affected by a slow-growing cancer.
It’s obvious (to me at least) that prostate cancer screening should be routine for all men after age 55, yet the USPSTF has retreated from recommending standard screening to recommending “watchful waiting” for most men. A potential result of that retreat is that the rate of metastatic prostate cancer has increased, requiring much more invasive surgery.
Which is to say, it’s better to get the bad news and do something about it (if possible) than to ignore it and go on your merry way – until something bad happens.
So that’s my excuse for leading off with a few bits of not-good news.
A link between ultraprocessed foods and colorectal cancer
Ultraprocessed foods refers to ready-to-eat foods that often contain high levels of sugar, salt, saturated fat, and food additives. Many packaged food products fall into the ultraprocessed category. A study conducted at Mass General Brigham Cancer Institute found an association between ultraprocessed foods and a significantly elevated risk of early-onset colorectal cancer.
The researchers analyzed data from the Nurses’ Health Study II, a long-term study of female nurses who were born between 1947 and 1964, which we have referred to in previous posts. They analyzed 24 years’ worth of data from 29,105 female nurses who received at least two colonoscopies before they turned 50 to screen for colorectal cancer precursors. The participants in the study had also completed dietary surveys every four years, from which the researchers estimated their average daily intake of ultraprocessed food. Although the diets of the study subjects were self-reported, this type of survey has been validated for its ability to accurately reflect a person’s dietary patterns.
On average, participants consumed 5.7 servings of ultraprocessed foods per day, which amounted to 35% of their total daily calories. This is slightly lower than the national average in the U.S.
From the endoscopy results, the researchers identified 2,787 participants who developed precursor polyps for colorectal cancer. Women who consumed the highest amounts of ultraprocessed foods — 10 servings per day on average — had a 45% higher risk of developing conventional adenomas, the precursor most associated with early-onset colorectal cancer, compared with those who consumed the lowest amounts (three servings per day on average).
There are other risk factors for colorectal cancer, such as such as body mass index, Type 2 diabetes, and low fiber intake. Even after accounting for all these other risk factors, the association of colorectal cancer with ultraprocessed foods was still statistically significant.
Please note that what the study identified were conventional adenomas. These can be identified in colonoscopies, and can frequently be removed during the colonoscopy. However, colonoscopies are infrequent in women under the age of 50. I am dubious as to the likelihood of a recommendation that relatively young women undergo colonoscopies, unless there is a clear symptom that suggests it. If the study has any implication, it would likely be that women – and not only women – limit consumption of ultraprocessed foods.
The incidence rate of colorectal cancer in men has historically been about a third higher than that in women, but that gap in rates has narrowed over time. Recent data indicates that colorectal cancer rates in women have slightly exceeded the rates in men. The factors have not been precisely defined, but lifestyles in both men and women have changed considerably over time.
The study was part of PROSPECT, from the Cancer Grand Challenges team, led by Professor Andrew Chan from Mass General and Dr Yin Cao of Washington University in St, Louis, published in JAMA Oncology in November. (JAMA Oncol. 2025 Nov 13:e254777. doi: 10.1001)
A factor not mentioned in the study is that both in the US and globally, women’s life expectancy is about six to seven years greater than men’s, thus, women have a greater likelihood of developing cancer simply because they live longer. The reasons usually given for this mostly have to do with lifestyle – for example, that men are more apt to behave violently, drive carelessly, and smoke.
I have to add that I am somewhat dubious about life expectancy data. E.g., life expectancy in the population segment labeled Hispanic in the US is about two-and-a-half years greater than in the non-Hispanic white segment. Lifestyle factors are cited as primary reasons. But it’s evident to me, at least, that a major factor is that a large segment of the Hispanic populace consists of immigrants, which means that many of these individuals were born outside the US. And since infant mortality rates are about double the overall mortality rate – 5.6 deaths per 1,000 births, versus the general mortality rate of 2.7 deaths per 1,000 persons, the Hispanic population’s death rate does not include all of the infant mortality data, resulting in a distortion of the data.
Tattoos pose significant health risks
One would think that it would be obvious that piercing our skin multiple times over fairly large areas and injecting a foreign substance under our skin is not healthy. Nonetheless, about a third of adults in the US have a tattoo, and more than a fifth of people in the US have more than one tattoo. Tattooing is more common in the younger cohorts than in individuals over the age of 65. According to data from the Pew Research Center, 41% of the US population under age 30 has a tattoo, and 46% of persons between 30 and 49 years old have tattoos, compared to 25% of the 50 to 64 cohort and 13% of the 65-plus cohort. Surprisingly, more women than men have tattoos – 38% versus 27%. The percentages of tattooing by ethnicity are surprising as well: 39% of African-Americans, 35% of Hispanics, 32% of Whites, and 14% of Asian Americans have tattoos. And the trend is rising, increasing from 21% of US adults in 2012 to 30% in 2019 and 32% in 2023.
Previous studies have pointed out the potential toxicity of tattoo ink, but no data has up to now indicated that tattooing is associated with specific adverse effects on health. The current study does identify specific health risks from tattoos, but only in mice.
The mice in the study we’re discussing had been tattooed as a way to identify them while they were being used in experiments. The scientists were first intrigued when they noticed that mice which had been tattooed for other experiments developed signs of inflammation. They then decided to investigate the effects of the tattoos themselves.They used standard black, red, and green ink to tattoo the skin on the hind feet of mice. They observed that the ink rapidly travelled along the lymphatic vessels to nearby lymph nodes, where it accumulated.
Specific effects observed by the researchers were that the tattoo ink appeared to affect the mice’s responses to vaccination. For example, mice injected with the Covid-19 vaccine demonstrated a reduced response to that vaccine – i.e., the vaccine’s effectiveness was adversely affected by the vaccine. On the other hand, the response to inactivated influenza vaccine was actually enhanced.
Researchers also found that the animals demonstrated chronic inflammation in their lymph nodes that was “acute and long-lasting”; the death of macrophages (a type of white blood cell); and altered immune response to other vaccinations.
The researchers concluded that an urgent concern associated with the safety of tattoos was that the ink from the tattoo site would be redistributed to other sites via the lymphatic vessels, where the accumulation of these insoluble pigments might have toxic effects. The researchers noted that the tattoo ink remained in the mice’s lymph nodes for the balance of their lives, with likely adverse effects on organs beyond the skin.
It’s highly unlikely that any data showing harmful effects of tattoos on mice would discourage humans from getting tattooed. But individuals getting tattooed should be made aware that the risk of hepatitis C increases by about 200% and of hepatitis B by 50%. Whether the new data demonstrating the penetration of tattoo ink to the lymphatic system will have any impact of the popularity of tattooing is doubtful, but at least it should be known in the Gumshoe world.
Obese persons may be at higher risk from Alzheimer’s disease
A study presented on December 2 at the annual meeting of the Radiological Society of North America (RSNA) in Chicago reported that the blood biomarkers of Alzheimer’s disease (AD) increased 95% faster in obese individuals than in persons without obesity.
The study investigated five years of data from 407 participants in the Alzheimer’s Disease Neuroimaging Initiative – in particular, positron emission tomography, (PET) scans, and blood samples.
The researchers assessed the association between AD biomarkers and body mass index (BMI). When the participants were first measured, a higher BMI was associated with a lower concentration of AD blood biomarkers. This was probably due to blood dilution, since people with higher body weight often have larger blood volume. But when the researchers followed the same participants over a longer period, they found that obese individuals had a higher proportion of AD biomarkers than normal-weight individuals. The PET scans in obese persons showed a buildup of amyloid plaque in their brains. Amyloid plaque, as we have often discussed, is one of the central hallmarks of dementia, including AD.
If obese individuals are at higher risk for AD, it might be reasonable to expect that drugs that treat obesity by dialing down appetite would reduce the risk of AD. In fact, some recent clinical trials (EVOKE and EVOKE+) are exploring whether weight reduction GLP-1 drugs such as semaglutide (Ozempic) could slow cognitive decline in people already diagnosed with early AD. (Cummings Jl, Alzheimers Res Ther. 2025 Jan 8;17(1):14)
A limitation of the finding that obesity is related to dementia is the fact that not all body fat carries the risk of AD. The research thus far strongly suggests that it is belly fat, rather than fat deposits under the skin, that is most directly related to the impact of obesity on the brain.
Other risk factors that often coincide with obesity — such as diabetes, hypertension and inflammation — may also contribute to Alzheimer’s biomarker changes. The researchers pointed out that the study sample was relatively small and specific, and may not represent the general population. The study also relied on observational data, which can reveal associations but does not prove that obesity directly causes faster AD pathology.
As with many early studies, this initial research points to the need for larger studies in more diverse populations with longer follow-ups. The lead author of the study, Dr. Soheil Mohammadi, a post-doctoral research associate at the Mallinckrodt Institute of Radiology, said “Our study shows that over a five-year period, obesity is associated with a steady increase in Alzheimer’s-related pathology. What surprised me was how sensitive the blood biomarkers were in detecting this relationship. They captured subtle changes even better than brain imaging.”
As most of us know, Alzheimer’s disease has a colossal impact on the human population of our planet. It’s estimated that about 55 million unfortunate people currently live with some form of dementia, AD being the most common. That prevalence is expected to increase enormously to more than 150 million by midcentury, unless a significant medical breakthrough emerges. AD is by far the most common form of dementia, accounting for about 60% to 70% of all cases. And it is also, by far, the leading cause of disability in the elderly population. As the population ages, the impact of Alzheimer’s grows. If obesity is a contributor to this global problem, it is one more reason to urge people to attempt to control their weight!
A decline in a person’s credit score is linked with an increase in cancer mortality
In other words, bad news is linked with more bad news. These findings, not yet peer-reviewed, were presented this past October at the American College of Surgeons Clinical Congress by Dr Benjamin James, chief of general surgery at Beth Israel Deaconess Medical Center and an associate professor of surgery at Harvard Medical School. The relationship between the credit scores and cancer mortality was based on clinical data from roughly 90,000 cancer patients in the Massachusetts Cancer Registry together with financial information from a national credit bureau.
The researchers adjusted for mortality-dependent variables, such as cancer type and stage, socioeconomic status, and race, and divided the credit scores into four tiers – 300-600, 600-660, 660-780, and 780-850. They found that patients who experienced a drop of two tiers within a year were 29% more likely to die. For those who experienced a two-tier drop within six months, that number increased to 63%.
The crucial question the investigators were investigating was the impact on a patient’s long-term survival if he/she is experiencing financial toxicity. As an example, if a person receives a medical bill that he/she cannot pay, or can only pay by refinancing his/her home, is that more likely to cause the person to die of cancer than if he/she did not have that debt?
The investigators observed that a credit score is a good marker of an individual’s overall financial health. And, crucially, it changes over time.
The study attempted to answer three questions: First: What is an individual’s mortality risk based on his/her cancer diagnosis and the credit score at the time of diagnosis? Unsurprisingly, they found that patients with a lower credit score at baseline were more likely to die. That finding relates to social determinants of health. Patients that are in the lower economic brackets, and are also in racial minorities are at greater risk of death. Sadly, that’s not a new finding.
The second question: Regardless of where a patient’s credit score starts, if that score drops or increases in the twelve months after diagnosis, how does that impact his/her mortality? The researchers adjusted for all those social determinants of health and focused on the credit score. What they noted was that when a patient’s credit score dropped by two tiers, that patient’s mortality risk increased by nearly 30%.
The third question focused on how that credit score changed over a six-month period. The investigators noted an even bigger change – i.e., a two-tier drop was associated with a 63% increase in cancer mortality. In other words, the same cancer diagnosis is associated with 63% higher probability of death, apparently based on a large drop in the patient’s credit score.
The obvious reason is that the patient in question is getting less care simply because he/she cannot afford to pay for it. Poor persons get less medical attention, such as annual physical examination. They likely seek care only when illness becomes acute, and the medical care they actually get is probably not of the quality accorded to the better-off.
Another potential explanation is that persons in the late stages of a disease like cancer may be in palliative care and not working, so that their credit score declines.
From my perspective, it is not very difficult to pick which is the cause and which is the consequence. It’s possible that a declining credit score is somehow a factor that accelerates the end of life. But it’s far more likely that as a person’s state of health declines, whether from cancer or some other cause, that person is less able to maintain his/her financial security.
The researchers considered this possibility, but they minimized it. To quote one of the authors, “I don’t believe the latter is the main cause of what we’re seeing, however, because the vast majority of patients in the study do not have end-stage disease. We can’t tease out the causes in this current data set, but we’re currently doing a prospective study where we’re surveying patients over time and collecting their financial data at the end of the study. So it’s a combination of both objective and subjective financial toxicity, in order to understand how they correlate with each other. We’re at the very beginning stages of that research, but that’s ultimately the way we’ll find out what’s really going on.”
It was noted by the investigators that an improvement in a person’s credit score did not have an effect contrary to a diminishment in the credit score. They gave no specific reason, but said that their assumption was that when a patient had the financial resources to pay for medical treatment, he/she simply paid for the necessary treatment. Having a higher credit score did not induce patients to increase their medical treatment.
I’m reluctant to question the validity of this study. As we noted, it was based on data from a very large patient cohort – 90,000 individuals – and also from sound and reliable financial data. The conclusion, stated in the simplest terms, was that worsening health data went along with worsening financial data. To put it in even simpler terms, as a person became poorer, he/she also got sicker. But that’s pretty obvious.
A key issue that was not addressed in this study was whether the study subjects had some form of health insurance. If the decline in their credit scores was due to loss of employment, then probably they lost their health insurance as well.The link between health and wealth goes both ways. Poor people may be reluctant to seek medical attention for a range of reasons. Visits to the doctor might cost money, or they might require taking time off from work. A person in “dire straits,” as money shortages were often called, is less likely to have annual medical check-ups. Instead, these persons are much more likely to delay seeking medical attention until their symptoms are more severe, by which time the problem may be much more resistant to treatment.
Did this study report information that had not previously been generally well-known? Perhaps the relationship between poor financial health and poor physical health had been taken for granted for a long, long time, but what the study revealed was the severe consequences a large decline in finances had on life-expectancy – i.e., that a two-tier drop in credit scores in a six-month period was associated with a 63% increase in mortality during that period. One could say that a severe drop in financial stability was almost tantamount to a death sentence.
When the authors were asked if anything could be done to offset this grim equation, their answer was predictable. Government and public institutions should do more to protect the health of the populace. They did not go so far as to propose free health care for everybody, but they stressed that some form of public support was necessary. Here’s what Dr James said:
“I think it all comes down to policy reform. That’s ultimately what we can do about this. I don’t personally believe that when people have medical debt that they can’t pay, that that should translate into an impact on their credit score.Also, providing people with financial navigators at the start of their diagnosis is important. It’s very hard as a provider to have cost conversations with patients when they get diagnosed. You walk into the office, you get a cancer diagnosis, and you’re told that you have to start thinking about the finances of this as well, because it will impact your long-term survival.
People are making choices: Are they going to go into debt, or are they going to choose to not have the medical care that they need?”
To this I would add that untreated health conditions in the general population turn out to be exceedingly expensive. Untreated infectious diseases spread and infect more and more people. Late stage cancers are much more expensive to treat. Conditions that affect a person’s capacity to accomplish simple tasks become increasingly disabling and require increasingly expensive treatment. And many or most of those health conditions that are untreated in the earlier stages wind up getting treated in their later stages, often in hospital emergency departments. Is that economical? The answer is obvious.
And now, as I promised, a couple of distinctly positive news items.
A potential new way of targeting and killing cancer cells
The strategy relies on a metabolic process that is seldom discussed. The process is called ferroptosis, which is a form of cell death driven by excessive oxidation of the lipids in cell membranes. When this occurs, the cell’s structural integrity collapses, leading to cell death. Cancer cells rely heavily on antioxidant proteins to prevent ferroptosis, as do other cells.
Researchers have been looking into ferroptosis as a strategy to kill cancer cells. A particular focus has been ferroptosis resistance, which is to say the mechanisms through which cells, including cancer cells, protect themselves against ferroptosis. Metastatic cancer cells that have spread to lymph nodes survive by relying on a protein called ferroptosis suppressor protein 1 (FSP1).
Most of the research into understanding factors that drive ferroptosis has focused on discoveries made in cells grown in plastic dishes, i.e., in vitro. A study published in Nature this past November took a different approach, looking into how living cancer cells attempt to protect themselves against ferroptosis. The researchers specifically investigated metastasized melanoma cells in the lymph nodes of mice. They then tested the efficacy of new agents that inhibit FSP1 directly in the tumors.
The study found that inside lymph nodes, FSP1 is a key line of defense against cell death. When the researchers delivered the FSP1 inhibitors directly to the tumors, the tumors’ growth was sharply reduced. In comparison, they tested this same drug on melanoma in vitro and saw little impact on cancer cell death.
The researchers noted that, in addition to pointing to the potential effectiveness of FSP1 inhibitors as a cancer treatment, the study helps to reframe how scientists think about ferroptosis in cancer—not as a single, uniform process, but as one that depends heavily on the tissue context.
The study’s first author, Dr Mario Palma, said “Metastatic disease, not the primary tumor, is what kills most cancer patients. Yet little is understood about how cancer cells adapt to survive in organs such as lymph nodes. We discovered that niche features of the lymph node actively shape which antioxidant systems melanoma can use. That context-specific dependency had not yet been fully appreciated and suggests that, rather than trying to kill every tumor cell the same way, we can exploit the weaknesses that arise as cancer spreads.” (Nature 2025 Nov 5. doi:10.1038/s41586-025-09709-1.
The discovery that the ferroptosis suppressor protein protects cells, including cancer cells, and that the protection that FSP1 provides cancer cells can be nullified by FSP1 inhibitors if these inhibitors are delivered directly to the tumors in lymph nodes, may indeed point to an effective pathway to treat cancer. But if FSP1 inhibitors eliminate a defense mechanism that protects non-cancer cells, that puts a significant limitation on the use of that pathway as cancer treatment.
Using FSP1 inhibitors has a certain similarity to using common cancer chemotherapy. The effectiveness of chemotherapy agents relies essentially on the greediness of cancer cells. These drugs harm normal cells, but the normal cells absorb much smaller quantities than cancer cells. The dosage of the chemotherapy drugs is calculated such that cancer cells absorb sufficient quantities to lead to cancer cells death, while non-cancerous cells absorb much smaller quantities, which may lead to the common chemotherapy side effects, such as fatigue, nausea, vomiting, and hair loss. Thus far, there is no data on whether humans will tolerate FSP1 inhibitors and therefore whether these prospective agents will take a place in cancer treatment.
However, any new way to target and kill cancer cells is a highly welcome step forward in the quest to limit the deadly effects of cancer on our fellow humans.
A new drug may prevent obesity and its associated harms
So far, the drug has been tested in mice and in very preliminary human studies, so don’t look for it on the pharmacy shelves any time soon. But the upshot of the experiments with this drug is that the mice, even when fed a high-fat diet that usually leads to excessive weight-gain in mice, did not gain any weight. Whether this drug would have the same effect in greedy humans is not yet known, but the prospects are pretty good.
As we know, obesity is much more than an inconvenience that requires us to purchase larger-sized clothing and prevents us from displaying a svelte and attractive appearance. Obesity is actually one of the most challenging health issues worldwide. As of 2022 (most recent data available), over one billion of us on Planet Earth would be classified as obese, including about 16% of adults, and more than 160 million children. The figures for the US vary according to the source, but over all they hover around 40%. The health consequences of obesity are far from trivial. Obesity leads to diabetes and heart disease, which as we know lead to a heightened risk of mortality. And the impact on healthcare costs is significant.
By now, just about everybody knows about the new class of drugs that are used for managing Type 2 diabetes and also for combating obesity. These are the GLP-1 (glucagon-like peptide-1) class, which include semiglutide (Ozempic and Wegovy), and tirzepatide (Mounjaro and Zepbound). Glucagon itself is a vital hormone from the pancreas that raises low blood sugar by signaling the liver to release stored glucose. The GLP-1 agents essentially do the opposite. They stimulate insulin release by the pancreas to metabolize blood sugar levels after meals, which lowers blood glucose. They also suppress the production of glucose by the liver, so these agents have two ways to manage diabetes. In addition to their effects in controlling blood sugar, they have two mechanisms which are effective in promoting weight-loss. They act on the brain in a way that decreases hunger, and they also slow down the digestive process, keeping the stomach full and decreasing appetite in that way.
The potential benefits of the GLP-1 agents beyond controlling Type-2 diabetes and promoting weight-loss also include reducing the risk of heart attacks and strokes, and lowering cholesterol.
Like most medications, GLP-1 agents can cause adverse effects in some persons, including nausea, vomiting, diarrhea, constipation, and abdominal discomfort. Less common side effects include increased heart rate, dizziness, fatigue, and headaches. These side effects often diminish as the body adjusts.
However, alternatives or complementary treatments could further improve results and reduce side effects. Researchers may now have found such an alternative in a newly developed compound named SANA, related to the common pain-reliever acetylsalicylic acid, i.e., aspirin.
Scientists originally designed SANA, (5-(2-nitroethenyl) salicylic acid), to fight inflammation, a key factor in obesity-related illnesses. Early experiments revealed something completely unexpected: SANA prevented mice from gaining weight, even when eating high-fat diets.
The new compound, SANA, works in ways entirely different from the GLP-1 agents. SANA activates a process termed thermogenesis – the body’s process of burning calories to generate heat. Normally, thermogenesis involves a protein called UCP1 within mitochondria, the energy factories in cells. However, SANA stimulates thermogenesis without UCP1, using a molecule called creatine instead.
This distinct action means SANA specifically targets fat tissue, reducing the risk of overheating and cardiovascular stress seen in older thermogenic agents, which often employ ingredients like caffeine, green tea, or capsaicin,
The development of SANA required a rigorous Phase 1 clinical trial involving human volunteers. The trial tested the safety of SANA as well as the potential benefits. The study evaluated two different doses – a single dose ranging from 200 to 800 mg and multiple doses from 200 to 400 mg daily for 15 days. The trial subjects were healthy overweight or obese volunteers.
The results were encouraging. SANA was well tolerated; the subjects experienced no severe side effects. More important, those taking the highest dose showed decreasing insulin resistance and some weight loss within just two weeks.
SANA could become the first in a new class of obesity drugs, potentially complementing existing treatments like GLP-1 agonists. Because it uses a novel mechanism, it can combine with drugs like semaglutide, enhancing overall weight-loss effectiveness.
Moreover, unlike GLP-1 drugs that sometimes cause muscle loss, which is particularly concerning in elderly individuals, SANA specifically burns fat without affecting muscle mass.
The development of SANA also points to the more advanced science behind drug development. Whereas many or most of the drugs now on the market were discovered almost accidentally, current drug discovery investigates the effect of potential agents at the most basic level, i.e., the interactions between the candidate drug and the essential factors in our physiologic function. It signals a potential step forward in drug development: less reliance on trial and error and more on science.
The next step will be Phase 2 clinical trials, which will investigate SANA’s effectiveness in larger human populations. If the Phase 2 trials are successful, SANA might represent a significant advancement in obesity treatment, providing millions worldwide with a safer, more efficient way to manage weight and metabolic health.
* * * * * * *
In planning this issue based on recent developments, I had thought to cover about eight subjects, but as you see I only managed six. And I have a bunch more that might be of interest to Gumshoe denizens, so I will be back with more short bits.
In the meantime, I’m hoping for a good, healthy, and fortunate new year, and I wish the same or better to you all.
Best, Michael Jorrin (aka Doc Gumshoe)
[ed note: Michael Jorrin, who I dubbed “Doc Gumshoe” many years ago, is a longtime medical writer (not a doctor) and shares his commentary with Gumshoe readers once or twice a month. He does not generally write about the investment prospects of topics he covers, but has agreed to our trading restrictions. Past Doc Gumshoe columns are available here.]
