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10/20/2026

Importance of Hormones on Gut Health.

LEAKY GUT & and ESTROGENS (E2 and E3) and PROGESTERONE (P4): Why higher incidence of leaky gut as we age? S*x steroids and protective gut wall “adhesive proteins”.
You should know this stuff! Not many do!
Dr. Devaki Lindsey Berkson
Oct 20
Our amazing gut wall is crazily one cell thick.
Our gut wall is made up of enterocytes, shoulder to shoulder.
Enterocytes are specialized, column-shaped epithelial cells lining both small and large intestines.
Single-celled enterocytes make up about 80% of the cells in the small epithelium (epithelium or epithelial cells are cells that line hollow organs like our digestive tracts).
Their absorptive surface is enhanced by microvilli
This one single cell border divides the “outside” world (food and whatever bacteria etc. lives “on” it) and our “insides” of what gets ourselves, meaning into our blood stream..
It’s kind of hard to mentally grasp the vulnerability of the human gut wall because it is basically just one cell thick, made up of these single-celled enterocytes.
The enterocytes stand belly to belly. Shoulder to shoulder.
When food is not coming into us, the barrier should be “closed.”
Enterocytes are designed to “open” during meals to allow supposedly optimally digested food particles (like amino acids, dipeptides, and tripeptides) into our bloodstream.
Food bits this small are no longer “seen” by our bodies as “non-self” molecules that need to be fought off, but as “self” molecules that can travel far and wide to nourish our cells.
Healthy, adequate digestion breaks proteins down into dipeptides, tripeptides, and single amino acids to be absorbed into the bloodstream.
Gut wall zippers
After absorption, tight “adhesive junction proteins” (families of proteins called claudins and occludins and junctional adhesive molecules) act like biochemical “zippers” to close the gut wall back up and maintain the intestinal barrier.
Our gut wall, enterocytes, needs these adhesive proteins to “zip” the gut wall closed again after meals.
If this does not happen properly, “leaky pathways or channels” can develop.
Then, debris from incompletely digested food, bacteria, or molecules that can go rogue, like LPS, crossing over (translocating across) the gut wall and getting into our bloodstream.
Potentially causing all kinds of issues far and wide.
Open Gut Walls Leave Our Bloodstream Vulnerable to Debris
If our gut walls do not close properly after meals, “leaky pathways or channels” develop.
Then debris of not fully digested particles of food or bacteria or other molecules can go rogue.
Like LPS.
Lipopolysaccharides (LPS), also known as endotoxins, are naturally present inside the gut.
They are fundamental components of the cell walls of Gram-negative bacteria.
These bacteria—such as E. coli—make up a significant portion of your normal, healthy gut microbiome.
The presence of LPS in the gut lumen is completely standard.
However, the way your body handles it dictates whether it remains harmless or drives inflammation.
We hope our LPS will stay harmless.
How? It all comes down to the function of your intestnal barrier.
The Intestinal Barrier
Healthy epithelial cells (cells that line hollow organs inside the body, like the gut) are bound tightly together, acting as a strict security wall that prevents LPS from escaping the gut and entering your bloodstream.
This requires adhesive proteins.
These lean on hormones.

10/19/2026

https://www.designsforhealth.com/blog/cruciferous-vegetables-and-healthy-estrogen-metabolism-during-menopause?utm_campaign=Weekly%20Wellness&utm_medium=email&utm_content=444921513&utm_source=hs_email

Designs for Health's extensive line of nutritional products are created after extensive product research.

10/16/2026

FSH and Body Composition: A Missing Link in Midlife Weight Gain?
A woman's midriff as she pinches the skin of her waist
Examining the Relationship Between FSH, Adipose Tissue Remodeling, Lean Mass Decline, and Metabolic Health
Written by: Emily Hernandez, MS, CNS

Symphony Natural Health Science and Medical Team

Reviewed by Dr. Deanna Minich, PhD, MS, CNS, FMCP, FACN

FSH receptors have been identified in human fat cells, and animal studies show blocking FSH reduces body fat and increases calorie-burning activity—but human research on FSH and body composition points in genuinely different directions depending on the population and timeframe studied [1,2].
The menopausal transition often brings frustrating changes in body composition. Despite no major changes in diet or exercise habits, fat seems to accumulate more easily around the abdomen, and muscle mass becomes harder to maintain. In addition, metabolic health may shift. This has fueled widespread interest in metabolic interventions during menopause, from GLP-1 agonists to hormone therapy, yet the endocrine drivers behind these changes remain incompletely understood.
These changes have traditionally been attributed to declining estrogen. More recently, however, researchers have begun asking whether another hallmark of menopause—rising follicle-stimulating hormone (FSH)—may also contribute to these shifts.
Although FSH is best known for its role in reproduction, researchers have identified FSH receptors in several tissues outside the ovaries. This has prompted new questions about whether rising FSH may influence body composition and metabolism during the menopausal transition. Emerging evidence suggests that FSH may interact with adipose tissue, skeletal muscle, bone, and metabolic pathways, raising the question of whether it contributes to some of the body composition changes observed during midlife [1,2].
While much remains to be learned, FSH may represent an important—and often overlooked—piece of the metabolic puzzle during the menopausal transition.
Adipose Tissue Is More Than Fat Storage
Adipose tissue was once viewed primarily as a storage depot for excess energy. Today, it's recognized as an active endocrine organ that communicates with the rest of the body through hormones and signaling molecules, including adipokines [3]. Adipokines help regulate appetite, insulin sensitivity, inflammatory balance, energy balance, and communication with other organs throughout the body [3,4].
Different fat depots serve different functions, including energy storage, heat production, and metabolic regulation [3,5]:
White adipose tissue primarily stores energy and produces endocrine signals.
Brown adipose tissue specializes in thermogenesis, helping the body burn calories to generate heat.
Beige adipose tissue can transition toward a more metabolically active, calorie-burning state under certain conditions.
Adipose tissue may directly respond to FSH signaling. Researchers have discovered functional FSH receptors (FSHR) on human and animal adipocytes [1]. This finding has expanded interest in FSH as a potential regulator of fat storage, energy expenditure, and metabolic health.
How Might FSH Influence Fat Tissue?
Experimental studies suggest that FSH signaling may affect adipocyte function through several mechanisms.
At the cellular level, FSH appears to activate pathways that promote adipocyte differentiation and lipid storage while suppressing thermogenic activity [1,6]. FSH signaling has been associated with increased expression of genes involved in fat storage, including lipoprotein lipase (LPL), fatty acid synthase (FAS), and peroxisome proliferator-activated receptor gamma (PPARγ) [6,7]. Additionally, FSH signaling may reduce the activity of uncoupling protein-1 (UCP1), which is involved in heat production and energy expenditure within brown adipose tissue [6,8].
In an animal model of menopause, blocking FSH signaling reduced body fat mass, increased thermogenic gene expression, promoted the "beiging" of white fat, and increased overall energy expenditure [6,8].
To fully understand if the same mechanisms observed in animal and cell studies translate to humans, more clinical research is required
FSH, Visceral Fat, and Metabolic Health
The relationship between FSH and adiposity in humans is more complicated than the preclinical data suggest, with findings varying by population and by how long researchers follow women over time.
Several observational studies have reported associations between higher FSH concentrations and greater waist circumference, waist-to-hip ratio, and visceral adipose tissue accumulation [2,9]. Because visceral fat is strongly associated with cardiometabolic risk, these findings have generated interest in FSH as a potential contributor to metabolic changes during menopause.
However, other studies have reported seemingly opposite findings. In the Women's Health Initiative Buffalo OsteoPerio Study, higher baseline FSH levels were associated with lower measures of adiposity, including visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), body mass index, total fat mass, and percent body fat over as many as 17 years of follow-up [10].
Further studies have shown that women with higher body mass index (BMI) have lower circulating FSH levels after menopause. One explanation is that adipose tissue can convert androgens into estrogens through aromatization, creating negative feedback on the pituitary gland and suppressing FSH production [11,12].
The relationship between FSH and adipose tissue is unlikely to be one-directional. Rising FSH may influence adipose tissue biology, but adipose tissue also feeds back into hormone regulation through estrogen production, making it difficult to separate cause and effect.
FSH, Adipokines, and Insulin Resistance
Researchers have also begun exploring how FSH may interact with adipokines—hormones released from adipose tissue that influence metabolism.
In postmenopausal women, FSH levels have been independently associated with adiponectin concentrations after adjustment for age, body mass index, and menopause duration [13]. Adiponectin plays important roles in insulin sensitivity, glucose regulation, and cardiometabolic health.
Additional studies have reported inverse associations between FSH and triglyceride concentrations during the menopausal transition [14]. Interestingly, clinical trials with FemmenessencePROTM demonstrated significant improvements in lipid biomarkers, including total cholesterol, LDL cholesterol, and HDL cholesterol [15,16]. At the time, these changes were largely attributed to the observed increases in estradiol. However, our evolving understanding of FSH biology invites a broader interpretation. Given that women taking FemmenessencePROTM also experienced significant reductions in FSH, it is worth considering whether some of the favorable cardiovascular effects may have been mediated not only by rising estradiol, but also by lowering FSH.
Relationships between FSH and fasting glucose have also been observed, although these associations often weaken after accounting for adiposity, which suggests that body fat may mediate some of the observed metabolic effects [14].
Rather than functioning solely as a reproductive hormone, FSH may participate in broader metabolic signaling networks.
Skeletal Muscle: Another Endocrine Organ
Body composition changes during menopause involve more than fat accumulation alone. Many women also experience reductions in skeletal muscle mass.
Skeletal muscle is also recognized as an endocrine organ. Muscle communicates with adipose tissue, bone, the liver, and even the brain through signaling molecules called myokines to help coordinate metabolism and energy balance [17].
Loss of lean muscle mass can contribute to changes in:
Bone health [18]
Immune function [19]
Insulin sensitivity and glucose regulation [20]
Metabolic rate [19]
Physical function [21]
Emerging evidence suggests that rising FSH may be associated with these changes. In a cross-sectional study of peri- and postmenopausal women aged 30-70 years, appendicular lean mass index was inversely associated with FSH concentrations, whereas no significant relationship was observed with estradiol or testosterone [22]. The prevalence of sarcopenia also increased substantially during the menopause transition, affecting approximately 30% of later perimenopausal women and 27-32% of postmenopausal women compared with only 3% of women in early perimenopause [22].
While these findings do not prove causation, they suggest that FSH may serve as a marker of broader musculoskeletal changes occurring during midlife.
Does FSH Cause Menopausal Weight Gain?
At present, the evidence does not support the conclusion that FSH directly causes menopausal weight gain. Much of the strongest mechanistic evidence comes from cellular and animal studies, while most human data remain observational. Additionally, findings are not always consistent across populations.
FSH appears to be one component of a much larger endocrine network that includes adipose tissue, skeletal muscle, ovarian hormones, aging, and lifestyle factors. More research is required to fully elucidate whether FSH actively contributes to body composition changes or merely reflects hormonal shifts during menopause.
"One of the biggest shifts we need to make in midlife nutrition is moving the conversation from weight to body composition. Preserving lean muscle, supporting metabolic flexibility, and maintaining healthy adipose tissue are far more meaningful goals than chasing a number on the scale. Understanding the hormonal environment, including FSH, may help us personalize those strategies."
Supporting Healthy Body Composition During Menopause
Several evidence-based strategies remain central for supporting body composition during midlife:
Encourage Resistance Training. Resistance exercise helps preserve lean muscle mass, maintain strength and bone health, and support metabolic health [23].
Consider Protein Intake. Dietary protein plays a key role in muscle protein synthesis and may help support lean mass when paired with resistance training [24].
Discuss Factors in Metabolic Health. Balanced nutrition, regular movement, and adequate sleep remain foundational for maintaining insulin sensitivity and metabolic flexibility [25,26].
Directly Target Endocrine Function. FemmenessencePRO™ has been shown to promote healthy function of the hypothalamic-pituitary-thyroid-adrenal-ovarian (HPTAO) axis, with favorable effects on key endocrine biomarkers, including reductions in FSH and increases in estradiol [15,16,27]. These hormonal changes have been associated with improvements in menopausal symptoms and a healthier body weight. By influencing this interconnected endocrine network, FemmenessencePRO™ may also promote healthy body composition, metabolic resilience, and whole-body adaptation during the menopausal transition.
Manage Chronic Stress. Supporting healthy stress resilience through adequate sleep, mindfulness practices, time outdoors, physical activity, or other stress-management techniques may help support overall metabolic and endocrine health [28,29].
Educate About Endocrine Disruptors. Emerging research suggests that endocrine disrupting chemicals (EDCs) may alter FSH-FSHR signaling and contribute to premature ovarian insufficiency [30,31]. Additionally, EDCs have been found to influence lipid and glucose metabolism and are associated with more adiposity [32].
Consider Shifting the Conversation from Weight to Body Composition. Changes in fat mass and muscle mass often occur independently of changes on the scale [33]. Waist circumference, strength, and body composition measurements may provide more meaningful insights than body weight alone.
"Nutrition and exercise remain the foundation of healthy body composition during menopause, but they're working within a changing endocrine landscape. Emerging research on FSH reminds us that muscle, fat, and metabolism don't respond to a single hormone. They reflect the integration of nutrition, movement, recovery, and the entire endocrine system."
The Bottom Line
As our understanding of menopause continues to evolve, researchers are looking beyond estrogen alone to better understand the hormonal changes that accompany this stage of life. FSH has become part of that conversation because of its potential connections to adipose tissue, skeletal muscle, and metabolic regulation. While many questions remain unanswered, these findings highlight the complexity of body composition changes during menopause and reinforce the importance of viewing them through a broader physiological lens.
Emily Hernandez
MS, CNS · Symphony Natural Health Science and Medical Team
Board-certified nutrition specialist. MS in Nutrition Education, American University. Practice focused on functional and integrative nutrition, with clinical emphasis on hypothalamic amenorrhea, PMOS, and healthy aging for athletes. Has presented research at scientific conferences, including a poster on Symphony's circadian health study and the data on Symphony's prostate product. Background in journalism and biology before clinical nutrition.
References
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Taneja C, Gera S, Kim SM, Iqbal J, Yuen T, Zaidi M. J Mol Endocrinol. 2019;63(3):R73-R80. doi:10.1530/JME-19-0152
Richard AJ, White U, Elks CM, Stephens JM. In: Feingold KR, Adler RA, Ahmed SF, et al., eds. Endotext. MDText.com, Inc.; 2020.
Clemente-Suárez VJ, Redondo-Flórez L, Beltrán-Velasco AI, et al. Biomedicines. 2023;11(5):1290. doi:10.3390/biomedicines11051290
Dowker-Key PD, Jadi PK, Alfatlawi R, Giannone RJ, Bettaieb A. Int J Mol Sci. 2026;27(4):1925. doi:10.3390/ijms27041925
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Cui H, Zhao G, Liu R, Zheng M, Chen J, Wen J. J Lipid Res. 2012;53(5):909-917. doi:10.1194/jlr.M025403
Kim SM, Sultana F, Sims S, et al. J Endocrinol. 2024;262(1):e230377. doi:10.1530/JOE-23-0377
Gavaler JS, Rosenblum E. J Am Coll Nutr. 2003;22(4):269-276. doi:10.1080/07315724.2003.10719303
Yue Y, Lima SM, Hovey KM, et al. Climacteric. 2026;29(3):409-415. doi:10.1080/13697137.2025.2595986
Ausmanas MK, Tan DA, Jaisamrarn U, Tian XW, Holinka CF. Climacteric. 2007;10(5):427-437. doi:10.1080/13697130701610780
Tepper PG, Randolph JF Jr, McConnell DS, et al. J Clin Endocrinol Metab. 2012;97(8):2872-2880. doi:10.1210/jc.2012-1422
Huang WY, Chen DR, Kor CT, et al. Metabolites. 2020;10(10):420. doi:10.3390/metabo10100420
Wang X, Zhang H, Chen Y, Du Y, Jin X, Zhang Z. J Obstet Gynaecol Res. 2020;46(8):1419-1424. doi:10.1111/jog.14297
Meissner HO, Mscisz A, Reich-Bilinska H, et al. Int J Biomed Sci. 2006;2(4):360-374.
Meissner HO, Mscisz A, Reich-Bilinska H, et al. Int J Biomed Sci. 2006;2(4):375-394.
Horváth L, Pekař M, Švagera Z, Horká V, Mráz M, Bužga M. Physiol Res. 2025;74(suppl 1):S37-S56. doi:10.33549/physiolres.935751
Bettis T, Kim BJ, Hamrick MW. Osteoporos Int. 2018;29(8):1713-1720. doi:10.1007/s00198-018-4570-1
Argilés JM, Campos N, Lopez-Pedrosa JM, Rueda R, Rodriguez-Mañas L. J Am Med Dir Assoc. 2016;17(9):789-796. doi:10.1016/j.jamda.2016.04.019
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10/16/2026

Testosterone info!!!
Testosterone’s signal are “globlal” even in women, especially in women. You want to know your levels of “free” T and SHBG (“ubers” that T rides through bloodstream) to keep healthy on many metrics.
Dr. Devaki Lindsey Berkson
Oct 16
Testosterone is “supposed to be” the most abundant biologically active s*x steroid in women and plays important roles across multiple physiological systems throughout the female lifespan.
Estrogen is in picograms inside the female body while BOTH testosterone (T) and progesterone (P) are in much larger amounts, in nanograms.
A nanogram is 1,000 times larger than a picogram (1 ng = 1,000 pg)
So some researchers and docs say that T levels are highest hormones in female body.
Some say P levels are.
Both are in nanograms.
Estrogen is in picograms.
Time will tell.
PS The above cited article is by one of my female hero’s Dr. Rebecca Glaser, the ex-breast cancer surgeon that has, through meticulous decades of human research, shown that lower T levels make women “more vulnerable” to breast cancer.
Her extensive work (along with her esteemed colleague Dr. Constantine Dimitrikakis) demonstrated that T (added to estrogen blockers in their research but perhaps not always the answer for “all” breast cancer patients, Jill C. and myself intend to hold a free sumitt on this on Valentine’s Day 2027 stay tuned) can greatly reduce suffering while improving breast cancer patient survival outcomes.
Both of these amazing agile thinkers have written and demonstrated this about testosterone in females:
Testosterone (T) therapy is being increasingly used to treat symptoms of hormone deficiency in BOTH pre and postmenopausal women.
Recently, especially with the advent of the T patch, additional research has been, and is currently being conducted on the safety and efficacy of T therapy. However, particularly in the United States (U.S.), there still exist many misconceptions about T and T therapy in women. This review addresses, and provides evidence to refute, some of the most common myths.
A major source of misconceptions regarding T therapy in women arises from epidemiological studies implicating elevated (endogenous) T levels with certain diseases. This data is misleadingly delivered to produce a pathogenic model of these diseases without enough evidence or plausibility to support a causative role. False conclusions repeated often enough, especially when supported with anecdotal observations, create ‘myths’ that become widely accepted, even in the absence of any biological or physiological rationale.
Another source of confusion concerning the safety of T therapy in both men and women is the extrapolation of adverse events (e.g., mental status changes, aggression, cardiac and liver problems, endocrine disturbances, abuse potential) from high doses of oral and injectable anabolic-androgenic steroids to T therapy, despite a lack of evidence. In this review, testosterone (T) refers only to bio-identical (human identical molecule) testosterone, not to oral, synthetic androgens or anabolic steroids.
In England and Australia, T is licensed and has been used in women for over 60 years.
However, as of 2013, in the U.S., there is no licensed T product for women and human/bio identical T is regulated as a ‘schedule 3’ drug and included as a ‘class X’ teratogen.
Yet:
While circulating testosterone (T) levels in women SHOULD BE 10 to 20 times higher than estradiol throughout their female life span, in today’s chemically exposed females, T levels are often way lower than they should be.
Why are T levels ideally supposed to be so high in females?...

10/12/2026

Celebrating Women in Pharmacy

10/12/2026

https://www.casi.org/articles/a-case-series-on-an-allulose-containing-gummy-in-healthy-adults-monitored-by-continuous-glucose-monitoring?utm_campaign=Weekly%20Wellness&utm_medium=email&utm_content=443520990&utm_source=hs_email

10/12/2026

https://www.designsforhealth.com/blog/how-your-gut-microbiome-influences-glp-1-appetite-and-metabolic-health?utm_campaign=Weekly%20Wellness&utm_medium=email&utm_content=443520990&utm_source=hs_email

Designs for Health's extensive line of nutritional products are created after extensive product research.

10/12/2026

https://www.designsforhealth.com/blog/glp-1-support-starts-with-daily-habits-nutrition-and-lifestyle-strategies-for-healthy-blood?utm_campaign=Weekly%20Wellness&utm_medium=email&utm_content=443520990&utm_source=hs_email

10/06/2026

Largest study to date: 1 million women followed for 20 yrs. of “oral” vs “topical” (patch) E2 tracking risk of stroke, heart attack and blood clots.
No contest. See which delivery mode is safest!
Dr. Devaki Lindsey Berkson
No more debate.

Does oral estrogen have the same risk of patch, gels, creams or pellets?

No.

It has much more!

A major Danish study published in the British Medical Journal on September 23, 2026, followed one million women for 20 years on oral vs. topical estrogen.

These Danish researchers found:

“Oral menopausal hormone therapy (1mg or more) increases risk - by 60% - for blood clots, stroke, and heart attacks, while transdermal therapies (patches, gels, or sprays) do “not” increase risk at all.

They also found:

Oral menopausal hormone therapy is linked to higher blood clot risk in legs or lungs ”regardless” of “dose” or “duration”.

But the increased risk of stroke and heart attacks were only seen with prolonged higher dose (1 mg of oral E2 or more).

Yet, transdermal hormone therapy (delivered via the skin as patches, gels, or sprays) showed no general increased blood clot risk.

I have been teaching this for years ever since the amazing French Esther studies showed this in the early 2000’s.

How did they run this study?

Danish researchers searched Danish health registry data for women aged 50-69 living in Denmark between 2003 and 2021 and diagnosed with a first venous thromboembolism, ischaemic stroke, or heart attack (myocardial infarction).

They identified 9,807 women with venous thromboembolism, 18,460 women with ischaemic stroke, and 11,974 women with heart attack.

These women were matched by birth year to a total of 49,035, 92,300, and 59,870 women without thrombotic disease, respectively.

Prescription records were then used to assess any links between hormone therapy use and thrombotic disease according to several variables including route of administration, dose, duration of use, and age treatment was started.

None of the women had a history of blood clots, cancer, liver disease, endometriosis, polycystic o***y syndrome, fertility treatment or surgery to remove ovaries (oophorectomy).

Other potentially influential factors such as income, education, medication use and pre-existing conditions were also taken into account.

Among women unexposed to hormone therapy, rates of venous thromboembolism, ischaemic stroke, and heart attack were 15.8, 20.3, and 13.0 per 10,000 person-years, respectively.

Oral oestrogen therapy (alone or with progestin) was associated with absolute increased rates of 0.09% for venous thromboembolism, 0.06% for ischaemic stroke, and 0.03% for heart attack per year.

This corresponds to one extra venous thromboembolism case per 1,055 women taking oral hormone therapy for one year, one extra stroke per 1,642, and one extra heart attack per 3,846.

Oral therapy was consistently associated with increased venous thromboembolism risk.

Whereas increased stroke and heart attack risks were confined to those taking high-dose oral oestradiol (above 1 mg/day) for more than a year, rising with longer use.

**** Transdermal therapy showed “no” general increased thrombotic risk regardless of regimen, dose, or duration.

One topical delivery exception:

When women combined transdermal continuous estrogen with synthetic progestins (as found in oral contreption and with IUDs) the risk of heart attack increased.

Synthetic progestins are bad news!

Stop the pill.

Stop the IUD.

Wonder why there is an epidemic of stroke, heart attack and clots in women in their 20’s? These synthetic hormones.

These synthetic hormones are handed out like M&Ms by OBGYNs to so many young women when natural progesterone will work better and be much safer.

But natural progesterone is NOT supported by Big Pharma.

While OBGYN associations are!

This is an observational study.

So the randomized trial freaks that proclaim no science means any science without randomized controlled trials, will screech to the heavens loud enough to break your ear drums.

Okay, so this study does not yet completely establish cause and effect.

Why or why doesn’t clinical acumen matter?

Yet, these authors say the large population design, use of detailed prescription data, the extensive health and sociodemographic information on the study population, and long follow-up suggest the results are “robust”.

Say that to your objecting gyn or urologist.

This BMJ Danish study finally concludes:

“Current use of any oral menopausal hormone therapy was associated with an increased venous thromboembolism risk, whereas ischaemic stroke and myocardial infarction risk was only increased with oral high-dose therapy used for more than one year.”

“Transdermal therapy was not associated with increased thrombotic rates regardless of regimen, active ingredients, dose, and duration of use.”

Knowledge is power.

Dr. B.