This Won't End Well... Seattle Becomes First City To Price-Fix Your Groceries

 by Mark Harmsworth via the Foundation for Economic Education (FEE)

This week the Seattle City Council passed Mayor Katie Wilson's "Fair Pricing and Transparency" ordinance in a 7-2 vote, a first-in-the-nation ban on so-called surveillance pricing.

The ordinance takes effect in 2027. The Washington Retail Association warned for months that the bill was rushed, would have significant and negative impact on prices, and that nearly all suggested fixes were ignored.

As approved, retailers must decide whether they can keep offering the tailored discounts and loyalty programs that Seattle families actually use or cancel all the programs and charge more for groceries.

Government should not be price-fixing consumer products.

Banning the use of loyalty cards and programs, fuel rewards, and targeted coupons hurts businesses and consumers alike.

Price controls do not make groceries cheaper. They flatten the tools stores use to compete for customers. When discounts vanish, the shelf price becomes the only price. That is how an "affordability" law raises a customer's grocery bill. A Greater Seattle Business Association and Seattle Latino Metropolitan Chamber guest column put it plainly: trying to control prices through experimental regulation has never worked, and this ordinance will make an already expensive city more unaffordable.

Jan Himebaugh of the Washington Retail Association offered a household example, nearly $1,000 in grocer loyalty savings this year for her family, the equivalent of more than 185 gallons of gas in a state where fuel is among the nation's most expensive. Those are not corporate talking points. They are the coupons that keep a cart full.

Thin-margin stores close. When they close, the result is the very "food deserts" Mayor Wilson has spent a campaign and a mayoralty promising to fight. Wilson has said Seattle will not accept food deserts as the cost of doing business, but the "Fair Pricing" policy creates a retail environment that does exactly the opposite.

A pricing ordinance that chases discounts out of the city works against that goal. You cannot subsidize corner markets on Sunday and make their discount model legally hazardous on Tuesday.

If Wilson wants more grocery access, the path is not to micromanage how a retailer prices a gallon of milk. It is to stop piling first-in-the-nation experiments onto businesses already carrying Seattle's tax and regulatory load.

Personalized discounts are not surveillance. They are how competitive stores keep prices down and stay open. Kill those discounts, and the desert grows.

https://www.zerohedge.com/political/wont-end-well-seattle-becomes-first-city-price-fix-your-groceries

Protein and Healthy Aging: Could Less Be More?

 Protein restriction, rather than higher-protein intake, could improve metabolic health in older adults and extend both healthy life expectancy and overall lifespan. This is the conclusion reached by Bailey Knopf, researcher, and Dudley Lamming, PhD, from the University of Wisconsin-Madison, in Cell Press Blue. In their review, the researchers examined published studies on protein restriction and identified six effects of reduced protein intake, along with the molecular mechanisms that may promote healthy aging. These benefits appear to be driven primarily by the restriction of specific amino acids, particularly methionine, leucine, isoleucine, and valine.

More or Less Protein?

Current guidelines, such as those from the German Nutrition Society, recommend a daily protein intake of 1.0 g/kg of body weight for adults aged 65 years or older, partly to reduce the risk for sarcopenia and frailty.

However, these recommendations contrast with epidemiologic findings. “Human association studies have found that high-protein diets are associated with an increased risk of diabetes, cancer, and mortality,” the authors wrote.

An analysis of data from the US National Health and Nutrition Examination Survey found that higher-protein intake was associated with increased mortality and age-associated diseases. A 2023 British twin study also found that higher-protein intake was positively associated with sarcopenia among older twins, challenging the conventional view that dietary protein prevents sarcopenia.

On the basis of these findings, Knopf and Lamming examined the potential benefits of reducing total protein intake while still meeting nutritional requirements, as well as the mechanisms that could explain these effects.

Six Key Effects

The researchers identified six major effects of protein restriction that may influence aging and age-associated diseases:

• Improved metabolic health
• Improved nutrient-sensing pathways (metabolic pathways that maintain the balance between energy production, storage, and consumption)
• Reduced cellular senescence
• Improved mitochondrial function
• Favorable epigenetic modifications
• Healthy aging

Effect 1: Improved Metabolic Health

Protein restriction improves metabolic function by reducing excess body weight, increasing energy expenditure, and improving glucose homeostasis. The authors noted that this effect was not caused by reduced calorie intake. Protein restriction can increase food intake while reducing fat mass and body weight because of increased energy expenditure.

Fibroblast growth factor 21 (FGF21), a hormone induced by nutrient stress, appears to be the primary mediator. FGF21 promotes energy expenditure and fat breakdown, increases insulin sensitivity, and exerts anti-inflammatory effects through several pathways.

Effect 2: Improved Nutrient Sensing

Protein restriction activates general control nonderepressible 2, an enzyme that detects amino acid deficiencies and suppresses protein synthesis. At the same time, the production of activating transcription factor 4 (ATF4) increases. ATF4 is a key regulator of the cellular stress response and promotes amino acid synthesis, autophagy, and antioxidant production.

Protein restriction also inhibits the mechanistic target of rapamycin complex 1 (mTORC1), a central protein complex involved in cell growth, energy metabolism, and protein synthesis. Inhibition of mTORC1 further reduces protein synthesis and activates autophagy.

Effect 3: Reduced Senescence

Cellular senescence is the irreversible arrest of the cell cycle. Senescent cells develop a senescence-associated secretory phenotype (SASP), activating proinflammatory signaling pathways that can contribute to tissue dysfunction and accelerate aging. Conversely, eliminating senescent cells may alleviate age-associated diseases.

High-protein diets increase senescence in the liver, whereas protein restriction reduces it. Studies have shown that FGF21 suppresses senescence in cultured cells and reduces the expression of proinflammatory SASP markers. Therefore, reducing senescent cells in metabolic tissues may contribute to the health benefits of protein restriction.

Effect 4: Improved Mitochondrial Function

Mitochondria become less efficient with age and produce more reactive oxygen species (ROS), which can damage cells, cause oxidative stress, and promote senescence. In the liver, ROS contribute to inflammation, fatty liver disease, fibrosis, and cancer. Mitochondrial dysfunction has also been associated with several age-associated diseases, including insulin resistance and type 2 diabetes. Protein restriction reduces ROS levels in the liver.

Studies in mice have shown that a high-protein diet significantly reduces electron transport chain activity in skeletal muscle and impairs exercise endurance. These findings suggest that high-protein intake could adversely affect mitochondrial homeostasis in skeletal muscle.

However, findings on the relationship between dietary protein content and mitochondrial function are inconsistent, and the authors noted that further research is needed.

Effect 5: Positive Epigenetic Modifications

Epigenetic modifications, including DNA methylation and posttranslational modifications of histones, influence which genes are active within a cell. Research suggests that protein restriction may promote a healthy lifespan by regulating the epigenome and preserving or restoring a more youthful epigenetic pattern.

Effect 6: Healthy Aging

Researchers noted that protein restriction can extend not only the lifespan but also the healthy lifespan across several species. A British twin study found that higher-protein intake was associated with an increased risk for sarcopenia, whereas a low-protein Mediterranean diet was associated with greater muscle mass and strength.

One possible explanation for these partly conflicting findings is the source of the protein. Plant proteins, unlike animal proteins, have been associated with a lower risk for frailty.

Research led by Lamming found that although a high-protein diet can promote muscle growth, particularly with strength training, restricting dietary protein or specific amino acids can reduce age-related increases in frailty in animal models.

Physical activity can largely offset the loss of lean body mass associated with low-protein diets in humans. This could potentially allow individuals to benefit from protein restriction while maintaining muscle mass.

The long lifespan of the Okinawa population has been partly attributed to a protein-restricted diet containing about 9% protein. Okinawa is one of the “Blue Zones,” regions where individuals live to an above-average age.

However, about 80% of the calories consumed by the Okinawan population come from plant-based sources, and the overall calorie intake is also lower. Therefore, the benefits cannot be attributed solely to lower protein intake. Nevertheless, these observations support the possibility that protein restriction promotes healthy aging in humans.

Resilience With Age

Physical resilience, or the ability to withstand and recover from stressors, such as extreme temperatures, fasting, and infections, decreases with age. Cellular resilience, which refers to the ability of cells to respond to stressors, such as hypoxia, pathogens, and heat, also decreases. Loss of resilience contributes to chronic diseases, multimorbidity, and death and is influenced by diet, lifestyle, and genetic factors.

In Drosophila, protein restriction increases resilience during aging and improves responses to starvation, bacterial infections, and heat stress. However, its effects on resilience in mammals remain unclear.

Specific Amino Acids

Numerous studies have examined the effects of restricting individual amino acids, although most have been conducted using animal models. These studies suggest that restricting essential amino acids (EAAs) can reproduce some of the lifespan benefits of general protein restriction, whereas restricting nonessential amino acids (NEAAs) does not appear to extend lifespan. Methionine and the branched-chain amino acids such as leucine, isoleucine, and valine appear to have particularly important effects.

Methionine restriction extends the lifespan of many species. Isoleucine restriction consistently improved metabolic health in mice across different diet and age groups. Valine restriction reduces body weight, improves metabolic health, and extends the lifespan of male mice.

NEAAs can also influence specific aspects of aging. Glycine supplementation extended the lifespan of mice by 6.2% in males and 3.7% in females, whereas tyrosine restriction significantly extended the lifespan of Drosophila.

Overall, the researchers concluded that NEAAs may be as important to the aging process as EEAs and should be considered individually. Supplementation with some NEAAs could promote healthy aging, whereas reducing the intake of others could have beneficial effects on health and longevity.

Implications for Practice

The authors cautioned against the rapid translation of these findings into clinical practice. Determining the optimal protein and specific amino acid intake for individual health remains challenging.

Particular caution is required in vulnerable populations. Pregnant women, children, individuals following calorie-restricted diets, and those recovering from illness could be harmed by protein or amino acid restriction. Many older adults have inadequate protein intake because of factors such as reduced appetite, financial constraints, and social isolation. Therefore, further restricting protein or amino acids could increase their risk for deficiency.

Individuals who exercise regularly may have higher-protein requirements or, at a minimum, may be able to consume higher amounts of protein or specific amino acids without an increased metabolic risk.

Researchers view these findings primarily as a basis for further research on the relationship between dietary protein and aging. The goal is to translate these findings into concrete, personalized dietary recommendations.

https://www.medscape.com/viewarticle/protein-and-healthy-aging-could-less-be-more-2026a10010nm

'Despite What Medspas Say, GLP-1s Are Not Beauty Products'

 Medspas profit by making people feel more attractive. That's their business model. Botox, chemical peels, and laser treatments exist to help women conform to cultural beauty standards that have long told us that our value rests on our appearance. Although that narrative hasn't done a lot for women (individually or collectively), everyone understands that a filler appointment is intended for cosmetic enhancement. 

An appointment to get a GLP-1 medication is something entirely different. 

The Evolution of Obesity 

Obesity is a chronic, relapsing, multifactorial disease often deeply intertwined with other chronic conditions. The field of obesity medicine has spent decades fighting to move treatment of this disease into the medical exam room — away from commercial entities profiting from an "eat-less, move-more" diet culture where excess weight is often treated as a character flaw rather than a manifestation of complex metabolic dysfunction. 

Instead of having obesity ignored or outsourced to commercial weight-loss programs, patients are increasingly hearing from clinicians that their biology is not a personal failing and are being offered evidence-based treatment. Some of this shift has undoubtedly been driven by pharmaceutical companies that have profited from the medicalization of weight management. Regardless, the change is long overdue.

Yet the system remains far from perfect. Clinicians bring varying levels of training and bias, and access to obesity care still falls short of demand. But we have finally begun to treat obesity as the chronic disease it is, within the framework of evidence-based medicine. 

Obesity Meds vs Beauty Products

At the same time, however, an alarming share of medspas across the country are dispensing GLP-1 medications almost like candy, folding them into the same beauty-industrial narrative that has marketed thinness as a measure of worth for generations, long before Ozempic existed. 

Many medspas are using compounded or otherwise non-US FDA-approved versions of these medications. Some offer doses and formulations that have not been validated or studied. They may combine them with vitamins or other agents without any evidence of their stability, compatibility, or clinical benefit. Patients may reasonably assume that these products have been evaluated in the same tightly controlled clinical trials that established the safety and efficacy of FDA-approved GLP-1 medications. Instead, they are the ones assuming the risks — if those risks are fully disclosed at all. 

This is not how evidence-based pharmacotherapy works. 

We would not tolerate this degree of unscientific extrapolation for other medical decisions, and for good reason. A drug studied in one population, at one dose, and in one formulation cannot automatically be assumed to perform the same way under different conditions. Yet that is precisely the assumption these clinics are running on, making everyone feel better by adding reassuring terms such as "microdosing."

The fact that this unconventional distribution model for obesity medication has failed to generate widespread outrage speaks to the stigma that continues to surround weight. It also reflects the lengths to which many people will go, and the risks they are willing to accept, to access treatment. People seek weight loss for many reasons. Some are cosmetic, and some are medical. Both deserve honest discussion, but they should not be conflated. 

Selling Thinness

When criticized, many medspas and direct-to-consumer prescribing companies argue that they are filling an important gap in the healthcare system by expanding access to life-changing medications that big pharma and insurers are selfishly stonewalling. If their primary mission truly was comprehensive obesity care, that argument might be honorable and compelling.

However, most of these for-profit companies are rarely, if ever, marketing treatment for a chronic disease. They are marketing thinness. 

This is made clear by simply looking at their advertisements. It's a 6-month "get-ready-for-swimsuit-season" campaign accompanied by images of thin women measuring their waists. It resembles crash dieting with a syringe instead of a meal replacement shake. The target market is not people struggling with disease. It is people who want to be more attractive.

Because nearly half of US adults have obesity, many of these businesses inevitably dispense GLP-1 medications to people who genuinely have the disease. What is less clear is whether they are also providing the less glamorous aspects of chronic disease management: titrating down a patient's diabetes medication as weight changes, monitoring body composition, managing side effects, or providing long-term follow-up.

Our Progress Is at Risk

This approach undermines decades of work spent establishing obesity as a legitimate disease that belongs in the halls of medicine and should be treated by trained clinicians. Every time a medspa markets a GLP-1 medication as another wellness upgrade, it reinforces the misconception that excess weight is fundamentally about willpower or vanity, and that any motivated business can "solve" it with the right product. That is precisely the framing our field has spent years trying to dismantle.

The implications extend beyond obesity medicine. If we hope to shift how women are valued — toward who they are rather than how they look — using a genuine medical breakthrough to reinforce the opposite message represents a significant step backward. Repackaging powerful obesity medications as the latest beauty trend only reinforces the longstanding equation of thinness with self-worth.

I do not believe most people operating these businesses intend to cause harm. More likely, they recognized a market opportunity and built businesses around it without asking whether a disease-modifying medication belongs in the same sales funnel as a lip filler. 

Intent, however, does not determine outcomes. 

Some patients who do not meet established clinical criteria are being started on these medications. Others who do meet criteria are receiving little more than a short-term weight-loss program instead of the comprehensive, lifelong management that obesity typically requires. It is essentially a large, unregulated human experiment, and it may take decades before the full consequences become apparent.

Two Futures for GLP-1 Medications

I suspect we are moving toward a world in which GLP-1 medications exist in two distinct spheres: one in which they are prescribed within medicine to treat a chronic disease, and another in which they are used by people without excess weight who are simply chasing a smaller body. 

The problem is that medspas are building the second sphere as quickly as they can while doing nothing to distinguish it from the first. The less those two uses appear to differ, the easier it becomes to conclude that obesity was never truly a disease in the first place. 

A field that fought this hard to establish obesity as a legitimate medical specialty deserves better than to be lumped in with the latest trend promising to make women smaller. More importantly, so do the patients these medications were developed to serve. 

https://www.medscape.com/viewarticle/despite-what-medspas-say-glp-1s-are-not-beauty-products-2026a100105x

'Statin Side Effects: What the Evidence Shows'

 The list of possible side effects attributed to statins is long: muscle pain, memory problems, depression, sleep disturbances, diabetes, and liver damage. However, a meta-analysis by the Cholesterol Treatment Trialists’ (CTT) Collaboration in The Lancet calls many of these associations into question. At the same time, the study confirmed that certain effects on muscles, the liver, and glucose metabolism can indeed occur. What matters, however, is their magnitude — and that is usually significantly lower than what the public criticism of these drugs would suggest.

Surprisingly Few Confirmed Side Effects

The new meta-analysis includes 19 double-blind, randomized, placebo-controlled trials involving 123,940 participants with a median follow-up period of 4.5 years. In addition, the authors evaluated four trials involving 30,724 participants in which more intensive statin therapy was compared with less intensive statin therapy.

They examined 66 adverse events listed in the package inserts for atorvastatin, fluvastatin, pravastatin, rosuvastatin, and simvastatin. Aside from the known effects on muscle function and glucose metabolism, only four of the 66 events remained statistically significant after adjusting for various confounding factors:

• Elevated transaminase levels
• Other liver function test values
• Change in urine composition
• Edema

Elevated transaminase levels occurred at a rate of 0.30% per year with statins and 0.22% per year with placebo. The relative risk (RR) was 1.41. Other abnormal liver function test values were observed in 0.25% of cases per year with statins vs 0.20% of cases per year with placebo. Changes in urine composition were observed in 0.21% of cases per year with statins vs 0.18% of cases per year with placebo, and edema was observed in 1.38% of cases per year with statins vs 1.31% of cases per year with placebo.

For the remaining 62 endpoints, there was no significant evidence of harm after statistical adjustment for potential confounders.

Memory and Cognition

Among the most common concerns expressed on social media is the fear of impaired memory and cognitive function. At first glance, this concern appears biologically plausible, given that cholesterol is essential for neuronal membranes and myelin. However, the brain’s cholesterol metabolism operates largely independently of peripheral low-density lipoprotein (LDL) metabolism.

Clinically, there is no convincing evidence of harm. The recent CTT analysis showed no robust association between statin therapy and cognitive impairment.

Another recent meta-analysis included 42 randomized trials involving 150,405 participants. For lipid-lowering therapies overall, the RR of neurocognitive events was 0.99 (95% CI, 0.88-1.12). For statins alone, the RR was 0.94 (95% CI, 0.72-1.25). No relevant negative effect was found in five specifically examined cognitive domains, namely attention, processing speed, executive function, working memory, and memory.

Depression and Sleep Disorders

Depression and sleep disorders are also often attributed to statins. However, both conditions occur frequently in the age group of patients typically prescribed statins. What matters, therefore, is not whether they occur during therapy but whether they are more frequent than without statins.

The new CTT meta-analysis found no evidence to support this. Neither depression nor sleep disturbances were significantly more common among statin users than among those taking a placebo. In the case of depression, observational data even pointed in the opposite direction.

A meta-analysis from 2025 included 15 studies from 10 countries with 5,403,692 participants. Statin users had a lower risk for depression, with a pooled odds ratio of 0.84 (95% CI, 0.74-0.96). However, the heterogeneity of the data was considerable. Therefore, no antidepressant effect can be inferred from these predominantly observational studies. However, they do not suggest a significant depression-promoting effect.

Muscle Pain

The situation is more nuanced when it comes to muscle pain. There is indeed a causal effect here, but the absolute magnitude is small.

The CTT Collaboration analyzed individual-level data from 19 placebo-controlled trials involving 123,940 participants. During a median follow-up of 4.3 years, 16,835 of 62,028 patients on statins (27.1%) reported muscle pain or muscle weakness. In the placebo group, the figure was 16,446 out of 61,912 participants (26.6%). The RR was 1.03 (95% CI, 1.01-1.06).

The difference was primarily concentrated in the first year of treatment. During this period, statins increased the RR by 7% (RR, 1.07; 95% CI, 1.04-1.10). In absolute terms, this corresponded to 11 additional muscle-related events per 1000 person-years. After the first year, no significant excess was detectable (RR, 0.99; 95% CI, 0.96-1.02).

The authors’ calculation is particularly illustrative: Of 15 muscle complaints reported by patients in the first year of statin therapy, statistically, only one was actually attributable to the medication. In the randomized trials, more than 90% of the muscle complaints reported by patients who were prescribed statins were therefore, mathematically speaking, not attributable to the statin.

'When Placebos Cause Almost as Many Complaints'

The SAMSON study demonstrated just how difficult the question of causality can be. The study included 60 patients who had previously discontinued statins due to side effects. They underwent 12 1-month phases: four with 20 mg of atorvastatin, four with a placebo and four without any medication at all. A total of 49 patients completed the entire study program.

Participants rated the intensity of their symptoms daily via an app on this scale:

• 1 = no or minimal symptoms
• 100 = maximum conceivable symptom intensity

The mean symptom score was 8.0 points during the months without medication. It increased to 16.3 points during periods when participants were taking atorvastatin, but it rose nearly as much — to 15.4 points — during placebo treatment. There was no significant difference between atorvastatin and placebo (P = .39). In other words, about 90% of the added symptom burden seen with atorvastatin, compared with that during the medication-free months, was also seen with placebo.

The larger StatinWISE study yielded similar results. Of 200 patients who had discontinued a statin due to muscle symptoms or intended to do so, 151 were included in the primary analysis. The difference in muscle symptom scores between atorvastatin and placebo was only -0.11 points on a 0-10 point scale (95% CI, -0.36 to 0.14; P = .40). Due to intolerable muscle symptoms, 9% discontinued treatment during the statin period and 7% discontinued treatment during the placebo period.

After the research team communicated the individual study results, 74 of 113 patients (65.5%) reported that they had already resumed statin therapy or intended to do so. After 15 months, 58 of 113 (51.3%) were indeed prescribed a statin again.

Why Statins May Affect Muscles

There is a biological explanation for why a small proportion of muscle symptoms are actually caused by statins. Statins inhibit 3-hydroxy-3-methylglutaryl coenzyme A reductase, thereby blocking the mevalonate pathway. This not only reduces cholesterol synthesis but also affects isoprenoid synthesis, protein prenylation, and coenzyme Q10 formation.

Discussions focus on changes in mitochondrial energy production, intracellular calcium homeostasis, and various signaling pathways in muscle cells. Mechanistic studies also point to possible effects on mitochondrial enzyme complexes and calcium ATPases.

However, the clinical data put these mechanisms into perspective: If 27.1% of patients on statins and 26.6% of patients on placebo report muscle symptoms, the impact on the mevalonate pathway cannot account for the majority of the observed complaints.

The same applies to coenzyme Q10. A decrease in its levels is biologically plausible. However, this does not mean that a Q10 deficiency is the most common cause of statin-associated muscle pain.

Diabetes

The evidence is clearer regarding glucose metabolism. Statins increase the risk for newly diagnosed diabetes, and the effect is dose dependent.

The CTT Collaboration analyzed 19 placebo-controlled trials involving 123,940 participants, as well as four dose-intensity studies involving 30,724 participants. Among patients on low- or moderate-intensity statins, 2420 out of 39,179 developed new-onset diabetes, compared with 2214 out of 39,266 in the placebo group. The annual rates were 1.3% vs 1.2%, corresponding to an RR of 1.10 (95% CI, 1.04-1.16).

With high-intensity statin therapy, the relative effect was greater: 1221 of 9935 patients on high-intensity statin therapy received a new diagnosis of diabetes compared with 905 of 9859 patients on placebo. The annual event rates were 4.8% vs 3.5%, with an RR of 1.36 (95% CI, 1.25-1.48). The metabolic shift itself was minor. Among participants without diabetes, mean glucose levels rose by only 0.04 mmol/L under low- or moderate-intensity statin therapy. The A1c level increased by an average of 0.06 percentage points and by 0.08 percentage points under high-intensity therapy.

Of note, approximately 62% of newly diagnosed cases of diabetes occurred in patients whose baseline glycemia was already in the top quartile. This suggests that the small increase in glycemia becomes clinically apparent primarily in patients whose baseline values are already close to the diagnostic threshold. For patients with high cardiovascular risk, however, the risk-benefit balance remains favorable.

Liver Enzymes

The liver is also an obvious target organ for side effects. This is where statins exert a large part of their effect: By inhibiting cholesterol synthesis, they increase the expression of hepatic LDL receptors, resulting in more LDL being removed from the blood.

It is well documented that laboratory values change. In the current Lancet analysis, 783 patients on statins showed elevated transaminase levels compared with 556 patients on placebo. The annual rate was 0.30% vs 0.22%, with an RR of 1.41 (95% CI, 1.26-1.57).

Other abnormal liver function tests were found in 651 vs 518 participants, corresponding to a rate of 0.25% vs 0.20% per year and an RR of 1.26. Taken together, this corresponded to an absolute annual excess of 0.13%.

The dose-response studies revealed a dose-response effect, further supporting causality. However, clinical interpretation remains crucial: An isolated elevation in transaminase levels is not equivalent to severe hepatotoxicity or liver failure.

Edema and Urinary Changes

Two lesser-known signals from The Lancet analysis are edema and changes in urinary composition:

• Regarding changes in urine composition, 556 events were documented in the statin group compared with 472 in the placebo group. The annual rates were 0.21% vs 0.18%, corresponding to an RR of 1.18 (95% CI, 1.04-1.33).
• Edema was significantly more common, but the difference between the groups was very small: 3495 patients on statins vs 3299 patients on placebo, corresponding to annual rates of 1.38% vs 1.31%. The RR was 1.07 (95% CI, 1.02-1.12).

Treatment Adherence Is Declining

The underlying problem: Both actual and perceived side effects are clinically relevant, because along with other factors, they can contribute to patients taking their statins irregularly or discontinuing their therapy altogether. Researchers distinguish between two terms:

• Adherence describes the extent to which actual medication use aligns with the prescribed dosing regimen. In many studies, a proportion of days covered or medication possession ratio of at least 80% is considered good adherence.
• Persistence, on the other hand, describes how long a patient continues therapy without discontinuing it or interrupting it for a predefined period.

There is significant room for improvement in both areas. A meta-analysis of 76 studies involving 5,898,141 patients found that only 62.4% (95% CI, 58.3%-66.5%) demonstrated good statin adherence. In primary prevention, the rate was 57.5%, and in secondary prevention, the rate was 64.4%.

The problem becomes even more apparent when it comes to persistence. In a German real-world analysis involving 865,732 patients, by day 300, approximately 71% had discontinued their statin therapy — as defined in the study — or had developed a treatment gap of the corresponding duration. After 36 months, only 20.6% remained persistent.

If symptoms are prematurely attributed to the statin, this can contribute to dose reduction or treatment interruption or discontinuation. Inadequate statin therapy, in turn, is associated with less favorable cardiovascular outcomes in observational studies. A recent systematic review on statin adherence and cardiovascular events confirms the link between higher adherence and lower cardiovascular risk. Thus, even supposed side effects can indirectly have clinical consequences.

Conclusion: What Does This Mean for Clinical Practice?

The current evidence paints a much more sobering picture of the side effect profile of statins than the long lists of possible complaints might suggest:

• Muscle symptoms may be causally related, but the absolute excess in the first year is approximately 11 additional events per 1000 person-years. In randomized trials, more than 90% of the muscle complaints reported by patients prescribed statins were, statistically speaking, not caused by the statin.
• Diabetes is a real, dose-dependent side effect. The RR of a new diagnosis increases by about 10% with low- to moderate-intensity therapy and by 36% with high-intensity therapy.
• Changes in liver function tests are also causal and dose dependent. However, the annual excess risk for abnormal liver function tests is only about 0.13%.
• In contrast, large, blinded randomized trials show no reliable increase in risk for cognitive impairment, depression, or sleep disturbances.

There is no question that statins can have side effects. Clinically, however, what matters is how likely it is that a specific symptom was actually caused by the statin — and how this risk compares with the cardiovascular benefits.

For this very reason, symptoms should neither be downplayed nor be hastily attributed to the statins. The practical challenge lies in recognizing genuine side effects, systematically investigating suspected side effects, and finding a lipid-lowering therapy that a patient will not only start but also continue long term.

https://www.medscape.com/viewarticle/statin-side-effects-what-evidence-shows-2026a100112s

'Message attributed to Khamenei praises Iran police chief'

 

Iran's Supreme Leader Mojtaba Khamenei praised police chief Ahmad Reza Radan as “brave and tireless,” honoring a commander with a long record of violent repression of protesters.

The message released by state media Saturday, but dated Thursday, October 8, and issued for National Police Week, praised Iran's police force as a pillar of national security and called for strengthening its capabilities, including the use of artificial intelligence.

Radan has been under US sanctions since 2010 for his role in the violent suppression of protests following Iran's disputed 2009 presidential election. The US Treasury held him responsible for police beatings, killings and arbitrary detentions, and cited allegations that he personally participated in abusing detainees at the notorious Kahrizak detention center, where protesters died in custody.

Since returning as national police chief in 2023, Radan has overseen the enforcement of compulsory hijab and successive crackdowns on Iranian protesters. During the 2026 nationwide protests, he warned that security forces had their “fingers on the trigger” against those taking to the streets.

https://www.iranintl.com/en/202610101133

Burnham: UK to adopt more Russia sanctions

 British Prime Minister Andy Burnham announced on Saturday that the United Kingdom will continue putting more pressure on Russia through sanctions and will take further action to "constrain the Russian war machine."

Following a conversation between Burnham and Ukrainian President Volodymyr Zelensky, the UK government said in a statement that both leaders stressed that Moscow should agree to an immediate energy ceasefire and stop its "brutal strikes" on Ukrainian infrastructure and shipping in the Black Sea.

"This would immediately release more energy and food supplies into the global market," Burnham and Zelensky emphasized, and agreed to meet in person in the coming days.

https://breakingthenews.net/Article/Burnham:-UK-to-adopt-more-Russia-sanctions/67271833

NJ Pulls More Improper Voter Registrations, Adds Daily Audits At Motor Vehicle Agency

 by Chase Smith via The Epoch Times,

New Jersey Gov. Mikie Sherrill on Oct. 7 ordered daily checks of voter registrations processed through the state Motor Vehicle Commission after a review found about 1,090 additional registrations that were improperly handled.

Sherrill ordered the review after disclosing in July that a software error had registered about 6,600 people who said they were not U.S. citizens when they applied for driver's licenses and state IDs between June 2023 and June 2024.

She said fewer than 400 of them voted.

Sherrill, a Democrat, said in a statement that neither of the new problems involved noncitizens.

About 750 of the records came from the same error in a system run by IDEMIA, the agency's vendor, according to a press release from the governor's office.

Those people answered "no" when asked whether they were old enough to vote, but their registrations went through anyway, her office said.

Sherrill's administration said their birth dates showed they were old enough and that many appeared to have pressed the wrong button on the keypad.

Because they answered no, the registrations weren't legally valid, according to the administration.

About 380 of those people had no other registration and didn't vote, and their records are being deleted, according to the governor's office.

About 320 voted and had other potentially valid registrations, and their cases are going to county election officials, the governor's press release stated.

About 50 were registered only because of the error and voted. Their records are being deleted and also sent to the counties. The other 340 records came from voter sign-ups at agency events for people leaving prison, dating back to 2016, Sherrill's office added.

The administration said some people at those events wrongly said they were eligible while still serving a sentence for an indictable offense, New Jersey's equivalent of a felony.

County officials will review those records one by one.

Separately, about 60 people were found to be currently incarcerated, and their names were sent to the counties for routine removal.

Under the new process, the agency will compare registration records each day against what customers actually entered, including citizenship, age, and whether they chose to register.

Records that don't match will be staff-reviewed before going to election officials.

The agency is also adding a keypad question at re-entry events asking people to confirm they aren't currently incarcerated for an indictable offense, and offering registration questions in five languages.

Sherrill said she promised a thorough review so that no ineligible person stays on the rolls and every eligible voter is heard.

"In just two and a half months, we conducted this review and are taking sweeping action," she said.

She criticized President Donald Trump, saying he has complained about the issue for a decade without fixing it.

State Senate Republican Leader Anthony Bucco said in a statement that the updates are "creating more questions than answers."

He said the public still hasn't seen the report on the original 6,600 registrations, and that with Election Day less than a month away, voters deserve to see the analysis behind the administration's conclusions.

Every Senate Republican has signed on to a resolution that would create a special Senate committee to investigate.

Bucco and state Sen. Kristin Corrado also introduced a bill that would end automatic voter registration at the agency, require voter ID, and set biannual independent audits of the voter rolls.

https://www.zerohedge.com/political/new-jersey-pulls-more-improper-voter-registrations-adds-daily-audits-motor-vehicle-agency