CLINICAL ASSOCIATION OF CALIFORNIA ENDOCRINOLOGISTS - EndoConnection.com
←
→
Page content transcription
If your browser does not render page correctly, please read the page content below
CLINICAL ASSOCIATION OF CALIFORNIA ENDOCRINOLOGISTS
https://endoconnection.com/ca
Dear CACE Members,
I hope that all of you and your families are safe and starting to live your lives with some
semblance of normalcy as we see increased vaccination rates for COVID 19. The past 18
months have definitely been a difficult time for all. This past year, the California Chapter of
AACE was dissolved and replaced by our new organization, CACE, the Clinical Association of
California Endocrinologists. Despite the initial jolt, we have landed on our feet, with a robust
online presence, advocacy, a career forum, and primary care symposia. We hope that our
virtual programs, including the updates on Medicare reimbursement and Telemedicine, as well
as our recent PCP programs, have been helpful to you and your primary care colleagues, as
well as providing continued value to your CACE membership.
It has been a very long time since we have seen our members in person—and I am excited to
remind everyone that our upcoming first annual CACE meeting is scheduled for September 24-
26, 2021 at the Hilton Torrey Pines in La Jolla, California. Our Annual Meeting program
committee, chaired by Drs. Jennifer Han and Adrienne Nassar, has created a meeting with an
outstanding line up of speakers and topics. I hope you will all sign up to join me; just go to our
CACE website at: https://endoconnection.com/ca/meetings/annual. Both CME and MOC credits
will be offered. At our business meeting held on Saturday morning, we will discuss in more detail
about the chapter dissolution by National AACE and the beginning of our own independent
association. If anyone is experiencing financial hardship, please do reach out to me so that we
can be certain to include you at a reduced rate. And, if you have a job opening or are looking for
a position, we will have a job fair midday Saturday!
With that being said, I look forward to seeing everyone in-person in September. If there are any
questions or concerns that arise before then, please feel free to reach out to me, as always. My
email address is: Jane.Weinreb@va.gov
All the best,
Jane
Jane Weinreb, MD
President, CACECACE 1ST ANNUAL MEETING
We are holding our 1ST Annual Meeting and Symposium for the Clinical Association of California
Endocrinologists on September 24-26th, 2021 at Torrey Pines Hilton in La Jolla, San Diego. The
agenda is packed with amazing speakers and we hope to see you there!
https://endoconnection.com/ca/meetings/annual/info
https://endoconnection.com/ca for registration!
CACE 2021 ANNUAL MEETING
September 24 - 26, 2021
Hilton La Jolla Torrey Pines
10950 N. Torrey Pines Road
La Jolla CA 92307
FRIDAY, SEPTEMBER 24, 2021
OVERVIEW
6:00 p.m. - 9:00 p.m. Registration / Information Desk
7:00 p.m. - 9:00 p.m. Exhibit Hall Open
GENERAL SESSION
7:00 p.m. - 9:00 p.m. Welcome Reception
SATURDAY, SEPTEMBER 25, 2021
OVERVIEW
6:30 a.m. - 6:30 p.m. Registration / Information Desk
7:00 a.m. - 6:20 p.m. Exhibit Hall Open
GENERAL SESSION
6:50 a.m. - 7:50 a.m. Industry Product Theater - Breakfast
8:00 a.m. - 8:10 a.m. Welcome Remarks
Speakers: Jennifer Y. Han, MD, FACE
UCLA South Bay Endocrine
Torrance, CA
Adrienne A. Nassar, MD, FACE
Kaiser Permanente
San Diego, CA
8:10 a.m. - 8:20 a.m. Pre-Meeting Assessment8:20 a.m. - 9:10 a.m. Use of technology to improve the lives of people with type 1
diabetes
Speaker: Steven V. Edelman, MD
Taking Control of Your Diabetes
Solana Beach, CA
9:10 a.m. - 10:00 a.m. CV Disease and Diabetes Update
Speaker: James T. Heywood, MD
Scripps Clinic John R. Anderson V Medical Pavilion
La Jolla, CA
10:00 a.m. - 10:30 a.m. AM Break / Visit Exhibits
10:30 a.m. - 11:20 a.m. An Endocrinologist's Guide to Satiety hormones (the
game changing obesity treatments have arrived)
Speaker: Ken Fujioka, MD
Scripps Clinic
Cardiff, CA
11:20 a.m. - 11:50 a.m. CACE Business Meeting
11:50 a.m. - 12:50 p.m. Industry Product Theater - Luncheon
11:50 a.m. - 12:50 p.m. Fellows Luncheon / Meeting
12:50 p.m. - 1:20 p.m. Dessert and Networking Break in Exhibit Hall
1:20 p.m. - 2:10 p.m. Diabetes in Times of Disaster
Speaker: Curtiss B. Cook, MD Professor of Medicine Mayo Clinic
Alix School of Medicine
Mayo Clinic Arizona
Scottsdale, AZ
2:10 p.m. - 5:10 p.m. Adrenal Symposium
2:10 p.m. - 2:50 p.m. Adrenal Incidentaloma: I Can See Clearly Now
Speaker: William F. Young, Jr., MD, MSc
Mayo Clinic Rochester
Rochester, MN
2:50 p.m. - 3:30 p.m. Hyperaldosteronism - Surgical vs. Medical Management
Speaker: Masha Livhits, MD, FACS
Endocrine Center
Los Angeles, CA
3:30 p.m. - 3:45 p.m. PM Break / Visit Exhibits3:45 p.m. - 4:25 p.m. Pheochromocytoma and Paraganglioma: Tips for the
Clinician
Speaker: William F. Young, Jr., MD, MSc
Mayo Clinic Rochester
Rochester, MN
4:25 p.m. - 4:55 p.m. Q & A
5:00 p.m. - 6:00 p.m. Reception
SUNDAY, SEPTEMBER 26, 2021
OVERVIEW
6:30 a.m. - 12:00 p.m. Registration / Information Desk
GENERAL SESSION
6:50 a.m. - 7:50 a.m. Industry Product Theater – Breakfast
8:00 a.m. - 8:10 a.m. Day 2 Welcome & Pre-Meeting Assessment
8:10 a.m. - 9:00 a.m. Female Infertility
Speaker: Andy Huang, MD, MBA, OBGYN, REI
Reproductive Partners Medical Group
Redondo Beach, CA
9:00 a.m. - 9:50 a.m. Hypogonadism & Reproductive Endocrinology from the
Perspective of a Reproductive Urologist
Speaker: James F. Smith, MD, MS
University of California, San Francisco
San Francisco, CA
9:50 a.m. - 10:05 a.m. AM Break
10:05 a.m. - 10:55 a.m. Management of Cushing Disease
Speaker: Laurence Katznelson, MD
Stanford University School of Medicine
Stanford, CA
10:55 a.m. - 11:45 a.m. Thyroid Cancer Guidelines Updates
Speaker: Susan J. Mandel, MD, MPH,FACE
University of Pennsylvania
Philadelphia, PA
11:45 a.m. - 12:00 p.m. Post Meeting Assessment
12:00 p.m. - 12:10 p.m. Closing Remarks & AdjournmentCA-AACE 2020 Annual Meeting Synopses of Presentations
Diabetes Technology Update—Timoth S. Bailey, MD, FACP, FACE, ECNU
Summarized by Mohammad Sadiq, MD (fellow, Edinburgh Centre for Endocrinology & Diabetes)
Diabetes success is easy but it’s the repetition and process of knowing your glucose levels and
modifying eating, exercise, emotion etc and doing these things every single day that creates
burden for people with diabetes. The role of diabetes technology is to achieve better outcomes
in terms of achieving lower HbA1c and lesser hypoglycemic risk with greater effectiveness and
less burden to the patient. This is possible with the newer insulins like inhaled insulins and
better delivery technology.
Insulin delivery options includes – “shoot, snort or pump” (patch or tethered) technology. The
“Achilles heel” of insulin pump therapy is the infusion sets. Multiple products are under
investigation to improve insulin absorption (e.g. multiple openings vs only a single opening at
the tip, catheters that resist kinking, and infusion sets that can last a full seven days. Adherence
is a major factor in achieving A1c goals. Adherence can be potentially improved by implantable
Continuous Glucose Monitors (CGMs), smart pens, and implantable drug pumps. FDA approval
has been secured for all but implantable insulin pumps. . Smart pen devices bring bolus
calculators to the MDI patient and basal titrators potentially increase the velocity to goal
achievement.
Glucose monitoring is a spectrum that includes – CGM, Flash Glucose Monitors (FGMs),
Professional CGM and Blood Glucose Monitors (BGM). The accuracy (as reflected by the mean
absolute relative difference (MARD) less than 10%) of the newer devices is better and
improved. Both CGM and FGM have been shown to improve both HbA1C and time in range
(TIR). In the real world setting, FGM has reduced the ketoacidosis and overall hospitalizations in
both type 1 and type 2 diabetes mellitus patient. This can happen as early as within six months
of onset and the trend continues to improve.
Emerging options to “cure” diabetes include automated insulin delivery (AID; or AP= “artificial
pancreas”) and cell therapy. The cell replacement system works on the principle that is it is
selectively permeable to the oxygen, glucose, and nutrients and impermeable to the immune
cells or is otherwise protected from immunorejection. The current AID systems include devices
with threshold suspend, fully-closed loop, and dual hormone systems. All of these show a
reduction in hypoglycemia, increased time in range and most an improvement in HbA1C.. The
controllers in AID systems are of two major types – model predictive control (MPC) and
proportional integrative derivative (PID). In a simpler sense the MPC uses an algorithm based
on predicted blood glucose in the next 30 minutes to adjust delivery, while PID uses information
from the past to adjust insulin delivery to achieves the glucose targets. DIY (“do it yourself”) AP
implements either MPC or PID controller algorithms, but has developed outside of FDA
regulations. It is limited to use by people with both advanced technical and diabetes care skills
and has no commercial support. However, endocrinologists need to be prepared to counsel
patients regarding its use.Only 21% of the type 1 diabetes adult achieve HBA1C less than 7%. Hence the need for
additional technologies that will allow more and more patients to achieve targets with less
hypoglycemic risk and burden. Although these technologies are useful, one needs to be mindful
regarding the human factor as not all patients are the same and also the safety of these
technologies are also an important consideration. More and more connected care and telehealth
are being used to give a unified care to improve the ease of achieving the target.
Thyroid Eye Disease—Raymond Douglas, MD, PhD
Summarized by: Sadiq Juma Al Lawati, MD, FRCPC (fellow, University of British Columbia)
Introduction:
Thyroid eye disease (TED) is most commonly associated with Graves orbitopathy. TED is a
manifestation of Graves disease (GD) in approximately 25% of patients. In those who develop
TED 80% will develop the eye symptoms within 18 months of GD diagnosis. TED is a serious,
progressive, and debilitating disease and it can cause irreversible damage. It is more common
in women, but men present with more severe disease.
Clinical features and complications:
TED has two stages, an active or inflammation phase in which there is tissue expansion and
remodeling in the orbit and the inactive or the fibrotic phase.
Symptoms and signs can include proptosis, eyelid retraction, strabismus, eyelid edema,
chemosis, and compressive optic neuropathy.
Complications can be divided into short-term and long-term complications.
Conjunctival chemosis
Short-term complications include:
Conjunctival redness
Photophobia and pain
Periorbital and lid erythema and edema
Lid retraction
Exposure keratopathy
Lid lag
Orbital ache
Lid retraction
Long term complications include:
Exposure keratopathy
Corneal ulceration
Severe dry eye (65%)
Proptosis
Retro-orbital ache
Strabismus
Diplopia (50%)
Color vision deficiency (7%)
Visual field defect (13%)Its important also to mention that TED is also associated with significant emotional distress
especially when the disfiguring signs are predominant.
Mild:
Grading system for TED:
o Retraction < 2 mm
o Exophthalmos < 3 mm
o Corneal exposure responds to lubricants
Moderate-Severe:
o Diplopia
o Exophthalmos > 3mm
o Retraction > 2mm
o Moderate-severe soft tissue involvement
Sight threatening:
o Corneal ulcer threatening breakdown
Treatment:
For active TED, options include local measures and observation, systemic steroids, biologics
and orbital radiation, while for the inactive phase, local measures and surgery are the usual
options.
There are medications that have been used to treat moderate-to-severe TED, these include:
Glucocorticoids:
o These medications do not reverse the underlying alterations of orbital tissue or
reverse proptosis or strabismus and have substantial side effects.
o EUGOGO regimen: Intravenous glucocorticoid therapy with a cumulative dose of 4.5g
of methylprednisolone divided over 12 weeks.
Rituximab:
o Chimeric mouse-human monoclonal antibody against CD-20 antigen on B
lymphocytes.
o Approved for many autoimmune conditions.
o Conflicting results from trials from moderate to severe TED with several reports of
development of dysthyroid optic neuropathy.
Tocilizumab:
o Humanized monoclonal antibody against IL-6 receptor.
o May have some efficacy.
Inhibits the proliferative response of T and B lymphocytes and recruitment of leukocytes.
MMF:
It targets mTOR pathways, having direct effect on orbital fibroblasts. A randomized control trial in 2018 with post hoc analysis showed reduction in relapse
Azathioprine:
rate after steroid withdrawal.
Fully human monoclonal antibody inhibitor of IGF-1 receptor. IGF-1 is overexpressed on
Teprotumumab:
Graves disease fibroblasts and immune cells. It blocks antibodies from attacking orbital
cells, therefore reducing inflammation and preventing excessive cell growth and
Approved by FDA in 2020.
hyaluronan build up behind the eye.
Phase 3 trial (OPTIC trial): primary endpoint: >= 2mm improvement in proptosis at week
24 was significantly greater with teprotumumab than placebo. There were secondary
Common side effects: mild to moderate side effects including muscle spasm, alopecia, GI
endpoints as well that were met too.
Summary of OPTIC-X and OPTIC 48-week off treatment results:
side effects.
o 89% of optic placebo patients achieved clinically significant proptosis reduction
when treated with teprotumumab in OPTIC-X.
o There were no new safety concerns in either OPTIC-X or 48-week OPTIC follow-
up period, even with the additional teprotumumab treatment in OPTIC-X.
Thyroid Eye Disease—Raymond Douglas, MD, PhD
Summarized by: Sophie M. Cannon, MD (PGY-3, UCSD Internal Medicine)
Thyroid eye disease (TED) is most commonly associated with Graves Disease (GD)
hyperthyroidism. Of the 25% of GD patients who develop TED, 80% develop TED within 18
months of GD diagnosis. TED is more common in women. The pathogenesis of TED includes
inflammation, tissue expansion, and remodeling in the orbit. Increased pressure in the fixed
bony orbit causes short-term inflammation with long-term consequences for delicate muscles
and connective tissue. As the connective tissue and adipose cells expand, this acute
inflammation can lead to fibrosis and thus irreversible proptosis within 1-3 years.
The clinical manifestations of TED are variable. Short term inflammation can lead to
keratoconjunctivitis sicca, photophobia, foreign body sensation, pain, periorbital lid erythema
and edema, lid lad, and orbital ache. Long term consequences include lid retraction, exposure
keratopathy, corneal ulceration, severe dry eye, proptosis, retro-orbital ache, strabismus,
diplopia, dysthyroid optic neuropathy, and even decrease in visual acuity, color vision
deficiency, and visual field defect. Of these symptoms, 65% of patients with TED experience dry
eyes, 50% experience diplopia, and 32% experience blurred vision. These consequences are
associated with significant emotional distress and disfigurement for patients.
Treatments for thyroid eye disease are largely limited. Until the recent development of
teprotumumab, there were no FDA approved treatments specific for TED. For active disease,there were local measures and observation, systemic steroids, biologics, and orbital radiation.
For inactive disease, local measures and surgery are indicated. Prior to teprotumumab, studies
of the aforementioned standard treatments were largely unremarkable. For the most part,
studies of glucocorticoids, rituximab, tocilizumab, mycophenolate mofetil, and azathioprine
exhibited no clinically significant changes in proptosis or strabismus. Outcomes were varied and
associated with significant side effects.
Thyroid eye disease is thought to be secondary to overexpression of insulin-like growth factor-1
receptor (IGF-1r). IGF-1r is overexpressed in Graves’ disease fibroblasts and immune cells, and
signaling of fibroblasts and immune cells mimics the pathologic findings seen in TED.
Teprotumumab is a fully human monoclonal antibody inhibitor of IGF-1r, and targets the binding
of IGF-1r to the IGF-1r/TSHr signaling complex. This blocks autoantibodies from attacking
orbital cells, and is thought to reduce inflammation and prevent excessive cell growth and
hyaluronan build up behind the eye.
Results from a large phase 3 peer-reviewed randomized controlled trial recently published by
Dr. Douglas in the New England Journal of Medicine (Teprotumumab for the Treatment of Active
Thyroid Eye Disease, NEJM 2020) describing the results of teprotumumab are promising.
Teprotumumab was compared to placebo (watch and wait), with a primary endpoint of >2mm
reduction in proptosis at week 24. The primary outcome of proptosis responders (>2mm
reduction) was significantly greater with teprotumumab than with placebo. Secondary endpoints
were also met, including but not limited to a clinical activity score reduction with participants
noting less spontaneous orbital pain, gaze evoked pain, eyelid swelling, eyelid erythema,
conjunctival redness, chemosis, and inflammation. Quality of life score improvements were also
noted. The most common adverse effects included muscle spasm and alopecia.
In conclusion, prior to teprotumumab, therapies for the acute inflammation associated with
thyroid eye disease were limited. A phase 3, placebo-controlled study demonstrated a
significant reduction in proptosis with teprotumumab. These results confirm that teprotumumab
is highly effective in reducing proptosis, supporting a positive benefit/risk profile in the treatment
of thyroid eye disease with apparent disease-modifying activity.
Dietary Management of Nephrolithiasis—Roger L. Sur, MD
Summarized by: Navya Reddy, MD (Fellow, Scripps)
This will be a brief synopsis of the metabolic management of kidney stones. It is important to
note that all patients with newly diagnosed stones undergo a screening evaluation with a dietary
medical history, serum chemistries, urinalysis, urine culture, as well as imaging. In addition, a
serum parathyroid hormone should be obtained if primary hyperparathyroidism is suspected in a
patient with high serum calcium levels, nephrocalcinosis, or with predominantly calcium
phosphate stones. Also, a stone analysis should be evaluated at least once if available. More
specifically, uric acid stones should be suspected with a low urine pH. In addition, struvite
stones are commonly seen with recurrent urinary tract infections. Cystinuria is commonly seen
in the presence of cystine stones. If there is evidence of calcium phosphate stones, we canconsider primary hyperparathyroidism, distal tubular renal tubular acidosis, carbonic anhydrase
inhibitors, or topiramate use.
Next we can discuss who should be evaluated for metabolic testing. Individuals should be
evaluated if they are recurrent stone formers, have a family history of stones, have a history of
bowel resection, suffer from gout, have type two diabetes, are obese, suffer from
nephrocalcinosis, have recurrent urinary tract infections, or participate in fad diets. Other relative
indications for metabolic testing include children or adolescents with kidney stones, patients with
solitary kidneys, or even patients who are interested in understanding why they have had
stones. Furthermore, medications that increase the risk of stone formation include zonisamide,
acetazolamide triamterene, probenecid, protease inhibitors, vitamin C, and topiramate.
Low risk ,first time, uncomplicated ,calcium stone formers should have a normal calcium intake,
have a modest oxalate restriction, reduce meat intake, restrict sodium in their diet, and have
high fluid intake. With this high fluid intake, patients should particularly restrict dark, sweetened
sodas. If a patient is found to have a kidney stone, metabolic testing should consist of one or
two twenty-four-hour urine collections obtained on a random diet. Specific urine testing should
also be done and includes a urine total volume, pH, urine calcium, UA, urinary citrate, urinary
oxalate, urinary sodium, urinary potassium, and urinary creatinine.
We can also discuss diet therapies that have been found to minimize kidney stone formation.
Clinicians should counsel patients with calcium stones and relatively high urinary calcium to limit
sodium intake and to not avoid calcium in their diets. A limitation of intake of non-dairy animal
proteins can help reduce stone recurrence. Patient should focus on a diet high in fruits and
vegetables. It is also important to note that foods high in alkali content increase urinary citrate
and that all forms of animal protein intake should be limited.
We can also explore the pharmacologic therapies associated with different kinds of kidney
stones. More specifically, if the patient has hypocitraturia with a urinary citrate level less than
500mg/day then we can treat the patient with potassium citrate. If the patient presents with
hyperuricosuria, we can treat the patient with allopurinol. In addition, if the patient is found to
have a gouty diathesis and an urinary pH less than 5.5 then we can treat them with potassium
citrate. Finally, patients with hypercalciuria with a urine calcium greater than 200, we can treat
with a thiazide diuretic. It is important to note that the common side effects of thiazide diuretics
include hypokalemia and hypocitraturia and that potassium supplementation may be needed for
some patients.
Dietary Management of Nephrolithiasis—Roger L. Sur, MD
Summarized by: Joseph Hsiao, MD (Fellow, UCLA)
Workup
All patients found with a new kidney stone should have a screening evaluation for causes of
increased stone risk. This should include a diet and medication history, as well as serum
chemistry-7, calcium, and uric acid. A urinalysis should be checked to evaluate pH and bacterial
content. Several commercially available panels are also available to assess for stone risk.Common associations to have in mind include:
Cystine stones = cystinuria
Uric acid stone = low urine pH
Carbonate apatite or Struvite stone (MgNHPhosphate)= Chronic UTI, urea splitting organism
Calcium Phosphate stone = primary hyperparathyroidism, distal RTA, Medullary Sponge
Kidney, carbonic anhydrase inhibitor, topiramate
A Renal ultrasound should be obtained, and a serum PTH should be checked if there is
suspicion for primary hyperparathyroidism (hypercalcemia, Calcium-Phosphate stones,
nephrocalcinosis on imaging).
When to obtain a 24 hour urine collection:
Absolute Indications: recurrent stone formers or high risk first time stone formers (+FH,
GI disease, hx bowel resection, gout, T2DM, obesity, nephrocalcinosis, recurrent UTI, fad
diet (high protein, high oxalate)
Relative Indications: child/adolescent, solitary kidney, or if patient requests further workup
Patient should do a random collection, and not vary diet during collection. This can be
repeated 1-2 times to ensure accuracy.
A 24 hour urine collection should include the following:
total volume, pH, calcium, oxalate, uric acid, citrate, Na, K, Cr
Optional: sulfate, cystine
Medications that increase the risk of stones include: vitamin C, acetazolamide, zonisamide,
probenecid, protease inhibitors, carbonic anhydrase inhibitors, topiramate
Treatment
Guidelines for management of Low risk, first-time uncomplicated stone formers of calcium
oxalate stones:
-Normal calcium intake 1000-1200 mg. Too little calcium can actually cause stone
formation
-Modest oxalate restriction (coffee, tea, spinach, peanuts). Can still have these on
occasion but keep consumption moderate.
-Meat less than or equal to 2 servings/day – each serving no bigger than deck of cards,
consider cutting down meat to twice a week
-Sodium restriction – very helpful, one of the more common causes of stones. Advise
patients to read labels and not to eat if salt is in first 3 ingredients. Ask for low sodium
when eating out
-High fluid intake – goal 2L urine per day – drink 100 oz of any fluid per day as long as it
is not dark colas or sugary drinks
Specific Diet therapies:
If hypercalciuria (>200 mg/day)- limit calcium to 1000-1200 mg/d
If excess sodium (>200 mEq/day)- this is a sign of too much sodium intake. Hypercalciuria will
improve with low sodium diet. Repeat urine collection after diet change to confirm progress.
If Hyperoxaluria – limit oxalate rich foods and maintain normal calcium intake. Calcium binds to
oxalate in gut and passes in feces, thus eliminating calcium from circulation. Yogurt is a goodsource of calcium and probiotics, maintain 1000 g/day calcium. Calcium tablets are a secondary option if unable to reach dietary goals. If low citrate with calcium stones – should increase intake of fruits and veg, limit non dairy animal protein. Foods with high alkali content increases urinary citrate If high uric acid in urine – decrease non-dairy animal protein (fish has highest source of uric acid) Medical therapies: If Urine Ca> 200 – decrease sodium, increase fluids, and start thiazide. Chlorthalidone 25 mg is the recommended starting dose, can increase to 50 mg as needed. Chlorthalidone is more favored than HCTZ. Watch for hypokalemia, which can cause hypocitraturia (repeat 24 hr urine after starting treatment). May need potassium supplement if citrate is low. If Citrate 600 mg/day (hyperuricosuria) – decrease meat, add allopurinol at 300 mg starting dose If pH
Negative calorie preloading is another effective strategy for weight loss by introducing a simple
dietary change. In negative calorie preloading, prior to a meal, individuals should consume
water, fresh fruits or vegetables before proceeding to the more calorie dense meal. By
preloading with low calorie density items, individuals consume fewer calories overall during the
meal. Dr. Greger reported that individuals can have a 44% greater decline in weight loss just by
drinking water before a meal.
Activated AMPK (adenosine monophosphate-activated protein kinase) plays a role in fat
metabolism, and can be activated through exercise, fasting, and nicotine. Dietary sources of
activated AMPK also exist, and an easy dietary addition is regular consumption of vinegar. The
acetic acid boosts AMPK in some tissues, and Dr. Greger discussed that apple cider vinegar
consumption can result in lost body fat and visceral body fat, without any other changes to diet.
He recommends two teaspoons of vinegar, such as apple cider vinegar, with each meal, and
suggests not drinking it straight and being sure to rinse out your mouth with water to protect
your tooth enamel.
Focus on fiber! Eating plant-based foods with green leafy membranes can increase fiber intake.
This type of plant-based fiber has numerous positive effects in the intestine. First, is the “ileal
brake” in which plant based fibrous membranes at the ileum change speed of absorption and
intestinal transit, and result in decreased food intake and a sensation of satiety. More distally in
the colon, plant-based fiber is critical to maintain healthy diverse gut flora.
Meat consumption, typically standard in the American diet, doubles the odds of becoming
overweight for school-aged children. Dr. Greger briefly reviewed evidence about poultry, red
meat and fish, to conclude that a vegan plant-based diet improves metabolic health. He
discussed that even an intermittently vegan diet can be beneficial.
And finally, Dr. Greger introduced the concept of “walling off your calories.” Plant cell based
foods have cell walls, which results in indigestible calories as some caloric content remains
trapped. When possible, he instructs us to consume the “fibrous wall.” In practice, this means
consuming whole grains, and minimally processed foods. Dr. Greger referenced the BROAD
study in which overweight individuals in New Zealand were randomized to standard diet vs
whole food based diet. With just dietary education alone, and encouragement to eat whole food
plant based diet (without restrictions on quantity of intake), participants lost weight and
maintained weight loss at 12 months.
To conclude, Dr. Greger emphasize the benefits of shifting towards a whole food plant-based
diet, supported by evidence with favorable results on caloric intake, weight loss, and metabolic
health.
Neuroendocrine Tumor Imaging—Richard J. Auchus, MD, PhD
Summarized by: Alexander Tyan (Fellow, UCSD)
Neuroendocrine tumors (NET) are tumors composed of cells with neurosecretory morphology
which can secrete hormones. They used to be called carcinoid tumors because they couldmetastasize but generally had indolent behavior with slow progression compared to other
cancers.
They are characterized by grade based on their mitotic index and stage based on extent of
spread of the tumor. They are also classified based upon their origin in the GI tract. The foregut
includes thymic NET, bronchial NET, small cell lung cancer, and pancreatic NETs. The midgut
includes small bowel carcinoids and we know the least about cancers originating in the hindgut.
Other NETs include pituitary adenomas/carcinomas, MTC, and pheochromocytoma/
paragangliomas. Unlike other malignancies, there is no correlation between NET stage and
grade; for example, you can have a stage 4 lesion but with a low grade. Diagnosis is through
tissue biopsy while imaging is only ancillary. Various tumor markers are associated with NETs.
Tumor burden can be assessed with chromogranin A and pancreastatin, prognosis with
neurokinin, and function with VIP and 5HIAA depending on the type of NET. Treatment for low
to medium grade tumors is surgery. Adjunctive therapies include radiofrequency ablation,
somatastatin analogs for widespread metastases, systemic chemotherapy, and DOTATATE-
Ytrittium or Lutetium which are beta emitters with tumorcidal effects. For high grade tumors,
treatment includes systemic chemotherapy with occasional radiation or local therapy.
Imaging modalities depends on the location and type of NET. Endoscopic ultrasound is
preferred for pancreatic insulinomas and gastrinomas except in MEN patients who have diffuse
gastrin producing cells. MRI arterial phase specifically protocoled for NETs can be useful to look
for liver mets due to “tumor blush” as NETs are very vascular. GA-DOTATATE is preferred for
metastatic disease while CT/MRI/Ultrasound are preferred for focal disease. For small bowel
NETs, GA-DOTATATE is superior to In-Pentotreotate. It is also more convenient as
pentrotretate requires imaging 24 hours after injection vs 1 hour after injection for DOTATATE.
In DOTATATE scans, pituitary and thyroid C-cells will light up due to the normal presence of
somatostatin receptors. In chronic inflammation, DOTATE can give false positives due to how
sensitive it is as macrophages also express somatostatin receptors. For pheochromocytoma,
MIBG is the preferred imaging modality. The overall takeaway point is that cross sectional
imaging is useful for anatomy while nuclear studies are useful for physiology.
Ectopic ACTH syndrome often presents acutely and is associated with hypokalemia,
hypertension, myopathy, neuropsychiatric symptoms, hyperpigmentation, irregular menses, and
weight loss/gain depending on its etiology. CT imaging is preferred to localize the tumor. In
ectopic ACTH syndrome, cortisol downregulates somatostatin receptors which can therefore
make ACTH secreting tumors difficult to pick up with octreotide based scans. Treating the
elevated cortisol levels which can be life threatening is often more urgent than treating the
cancer immediately.
2020 AACE/ACE Postmenopausal Osteoporosis Treatment Guidelines Updates—
Pauline Camacho, MD, FACE
Summarized by: Stephanie Kim, MD (Fellow, UCSF)Key updates in the 2020 AACE/ACE Postmenopausal Osteoporosis Treatment Guidelines include clarification of the diagnostic criteria, a new risk stratification criteria, inclusion of romosozumab in the treatment algorithm, and new guidance on transitioning/discontinuing agents (eg. denosumab). Osteoporosis is prevalent and the burden of osteoporosis is high. All postmenopausal women ≥50 years old should be screened for osteoporosis and fracture risk measured with tools like FRAX. BMD testing is recommended for all women ≥65 years old, all postmenopausal women with a history of fracture(s) without major trauma and high risk features, or those with secondary osteoporosis. Diagnostic criteria for osteoporosis is T score -2.5 or below at the lumbar spine, femoral neck, total proximal femur or 1/3 radius; low-trauma spine or hip fracture regardless of BMD; T-score between -1.0 and -2.5 and fragility fracture of proximal humerus, pelvis or distal forearm; and T-score between -1.0 and -2.5 with high FRAX. Evaluation for secondary causes of osteoporosis is important as it can be seen in up to a third of women with osteoporosis without major risk factors. Most common causes are hypercalciuria, malabsorption of calcium, hyperparathyroidism, vitamin D deficiency, hyperthyroidism, and Cushing’s disease. Lab tests to consider in detecting secondary osteoporosis include CBC, serum chemistry, 25-OH vitamin D, and 24 hour urine calcium, sodium and creatinine. Pharmacologic therapies are categorized into antiresorptive agents (bisphosphonates, selective estrogen agonists/antagonists, estrogens, calcitonin, denosumab), parathyroid hormone analogues (teriparatide and abaloparatide), romosozumab. Therapy is recommended for patients with T-score between -1.0 and -2.5 in the spine, femoral neck, total hip or 1/3 radius and history of fragility fracture at the hip or spine; T-score of -2.5 or less in the spine, femoral neck, total hip or 1/3 radius; and T-score between -1.0 and -2.5 if the FRAX 10-year probability for major osteoporotic fracture ≥20% or hip fracture ≥3%. Risk stratification is an important update for 2020. Examples of very high fracture risk include recent fracture within last year, fracture while on approved therapy, multiple fractures, fractures while on drugs causing skeletal harm, T-score
Therapy should be resumed after a bisphosphonate holiday if the patient has new fragility
fractures, a significant decline in BMD, or bone turnover markers that have risen to pretreatment
levels.
Romosozumab is a humanized monoclonal antibody that inhibits sclerostin, a protein secreted
by osteocytes to reduce bone formation. It is indicated for osteoporosis in postmenopausal
women at high risk of fracture or who failed or are intolerant of other therapies. Duration is
limited to 12 months. It is given as 2 subcutaneous injections totaling 210 mg once monthly.
There is a black box warning and it should not be used in patients who had an MI or stroke in
the previous year as there is a potential risk of MI, stroke and CV death. Romosozumab was
approved based on the FRAME and ARCH trials. In summary, romosozumab is recommended
for patients with very high fracture risk, previously treated with teriparatide or abaloparatide but
still need anabolic effect, on injectable antiresorptive therapy that are “failing” therapy.
Discontinuation from denosumab is not recommended without a proper transition plan. There is
a rapid decrease in BMD with discontinuation of denosumab after 2 or 8 years. BTM increase to
values above baseline by 12 months after discontinuation. Switching to injectable therapies:
First, assess for compliance and reevaluate for secondary causes. If the patient is on oral
therapy, switch to an injectable antiresorptive. If the patient is on injectable antiresorptive or at
very high risk of fracture, switch to abaloparatide, romosozumab or teriparatide. Transitions for
very high risk patients: If the patient is on denosumab, continue therapy until the patient is no
longer high risk and ensure transition with another antiresorptive agent. If the patient is on
romosozumab for 1 year/abaloparatide or teriparatide for up to 2 years, start sequential therapy
with oral or injectable antiresorptive agent. If the patient is on zoledronate and stable, continue
therapy for 6 years, but if there is progression of bone loss or recurrent fractures, consider
switching to abaloparatide, teriparatide or romosozumab.
2020 AACE/ACE Postmenopausal Osteoporosis Treatment Guidelines Updates—
Pauline Camacho, MD, FACE
Summarized by: Tina Mosaferi, MD (Fellow, UCLA)
Our annual conference started with a lecture by Dr. Pauline Camacho focused on reviewing the
American Association of Clinical Endocrinologists/American College of Endocrinology Clinical
Practice Guidelines for the Diagnosis and Treatment of Postmenopausal Osteoporosis-2020
Update (1).
54% of adults in the United States over 50 years of age suffer from osteoporosis or osteopenia
(2). This equates to approximately 10 million with osteoporosis and 43 million with low bone
mass (3)! The health and financial consequences of osteoporosis can be dire. According to a
Milliman research report commissioned by the National Osteoporosis Foundation, nearly one in
five Medicare beneficiaries died within 12 months of a new osteoporotic fracture in 2015 (4).
Care for osteoporotic fractures among Medicare beneficiaries cost about $57 billion dollars in
2018 (5). Despite the high prevalence and associated disease burden, there is evidence of ashocking treatment gap. The percentage of patients receiving a medication for osteoporosis
following a hip fracture declined from 40% in 2002 to 21% in 2011 (6).
Highlighting this notable epidemiology, Dr. Camacho delved into the 2020 AACE/ACE
Postmenopausal Osteoporosis Treatment Guideline Updates. Starting at a fundamental level,
the diagnostic criteria of osteoporosis were defined:
1. Bone mineral density (BMD) T-score -2.5 or below at the lumbar spine, femoral neck,
total proximal femur, or 1/3 radius;
2. Low trauma spine or hip fracture, irrespective of BMD findings;
3. BMD T-score between -1.0 and -2.5 and a fragility fracture of the proximal humerus,
pelvis, or distal forearm; or
4. BMD T-score between -1.0 and -2.5 and high FRAX fracture probability based on
country-specific thresholds.
Upon diagnosis of osteoporosis, the guideline updates suggest that all postmenopausal women
should undergo laboratory evaluation for secondary causes. This includes a complete blood cell
count; comprehensive metabolic panel; phosphorous; intact parathyroid hormone; Vitamin D 25-
OH; and a 24-hour urine collection for calcium, sodium, and creatinine. Particular attention
should be paid to disorders of calcium metabolism and hyperparathyroidism. Additional testing
is encouraged based on clinical suspicion, including but not limited to thyroid stimulating
hormone, celiac antibodies, and serum/urine protein electrophoresis.
With respect to treatment, AACE strongly recommends pharmacologic therapy for patients with:
1. BMD T-score between -1.0 and -2.5 in the spine, femoral neck, total hip, or 1/3 radius
and a history of fragility fracture of the hip or spine;
2. BMD T-score of -2.5 or less in the spine, femoral neck, total hip, or 1/3 radius; or
if the FRAX 10-year probability for major osteoporotic fracture (MOF) is 20% or the 10-
3. BMD T-score between -1.0 and -2.5 in the spine, femoral neck, total hip, or 1/3 radius
year probability of hip fracture is 3% (in the United States).
Once the need for pharmacologic therapy has been established, risk stratification is advised into
one of two categories: very high risk or high risk. Recent fractures (within the prior 12 months),
fracture while on approved therapy, multiple fractures, fractures while on drugs causing skeletal
harm, BMD T-score < -3.0, high risk of falls, or high fracture probability by FRAX (MOF>30%,
hip fracture >4.5%) are examples of patients who qualify for a very high fracture risk distinction.
Patients at very high risk for fracture may be started on abaloparatide, denosumab,
romosozumab, teriparatide, or zoledronate. Alendronate and risedronate are considered to be
alternate therapy for this group of patients. By contrast, patients at high risk for fracture are
advised to be started on alendronate, denosumab, risedronate, or zoledronate.
Following the start of pharmacologic therapy, yearly assessment is needed to assess calcium
intake and Vitamin D supplementation, fall risk, fracture occurrence, physical activity toleration,
and medication adherence. Annual fracture risk assessments alongside BMD trends and bone
marker data may be used to further tailor therapy. For example, patients who are no longer high
risk for fracture or have stable or increasing BMD on serial DXA scans may be considered for
bisphosphonate holidays. By contrast, denosumab treatment should not be discontinued withouta proper transition plan given the significant risk of rebound fractures (7). Therapy with an anabolic agent (abaloparatide, teriparatide, or romosozumab) should also be followed with either a bisphosphonate or denosumab to prevent bone density decline and loss of fracture efficacy (8, 9, 10). Notably, the updated guidelines do not recommend combination therapy for postmenopausal osteoporosis at this time until further data is available for review. Dr. Camacho’s lecture reinforced the significance of osteoporosis identification and evaluation, providing our meeting members with the updated tools necessary for providing guideline- directed care. References 1. Camacho PM, Petak SM, Binkley N, et al. American Association Of Clinical Endocrinologists/American College Of Endocrinology Clinical Practice Guidelines For The Diagnosis And Treatment Of Postmenopausal Osteoporosis—2020 Update. Endocrine Practice. 2020;26(Supplement 1):1-46. doi:10.4158/gl-2020-0524suppl 2. Wright NC, Looker AC, Saag KG, et al. The Recent Prevalence of Osteoporosis and Low Bone Mass in the United States Based on Bone Mineral Density at the Femoral Neck or Lumbar Spine. Journal of Bone and Mineral Research. 2014;29(11):2520-2526. doi:10.1002/jbmr.2269 3. NOF Releases Updated Data Detailing the Prevalence of Osteoporosis and Low Bone Mass in the U.S. National Osteoporosis Foundation. June 2014. https://www.nof.org/news/54-million- americans-affected-by-osteoporosis-and-low-bone-mass/. Accessed September 13, 2020. 4. Hansen D, Bazell CB, Palizzari P, et al. Medicare cost of osteoporotic fractures. Milliman Research Report. Commissioned by the National Osteoporosis Foundation. August 2019. http://assets.milliman.com/ektron/Medicare_cost_of_osteoporotic_fractures.pdf. Accessed September 13, 2020. 5. Lewiecki EM, Ortendahl JD, Vanderpuye-Orgle J, et al. Healthcare Policy Changes in Osteoporosis Can Improve Outcomes and Reduce Costs in the United States. JBMR Plus. 2019;3(9). doi:10.1002/jbm4.10192 6. Solomon DH, Johnston SS, Boytsov NN, et al. Osteoporosis Medication Use After Hip Fracture in U.S. Patients Between 2002 and 2011. Journal of Bone and Mineral Research. 2014;29(9):1929-1937. doi:10.1002/jbmr.2202 7. Cummings SR, Ferrari S, Eastell R, et al. Vertebral Fractures After Discontinuation of Denosumab: A Post Hoc Analysis of the Randomized Placebo-Controlled FREEDOM Trial and Its Extension. Journal of Bone and Mineral Research. 2017;33(2):190-198. doi:10.1002/jbmr.3337 8. Rittmaster RS, Bolognese M, Ettinger MP, et al. Enhancement of Bone Mass in Osteoporotic Women with Parathyroid Hormone followed by Alendronate. The Journal of Clinical Endocrinology & Metabolism. 2000;85(6):2129-2134. doi:10.1210/jcem.85.6.6614
9. Cosman F, Crittenden DB, Adachi JD, et al. Romosozumab Treatment in Postmenopausal
Women with Osteoporosis. New England Journal of Medicine. 2016;375(16):1532-1543.
doi:10.1056/nejmoa1607948
10. Leder BZ, Tsai JN, Uihlein AV, et al. Denosumab and teriparatide transitions in
postmenopausal osteoporosis (the DATA-Switch study): extension of a randomised controlled
trial. The Lancet. 2015;386(9999):1147-1155. doi:10.1016/s0140-6736(15)61120-5
2020 AACE/ACE Postmenopausal Osteoporosis Treatment Guidelines Updates—
Pauline Camacho, MD, FACE
Summarized by: Manita Choudhary, MD (Fellow, Cedars-Sinai)
Prevalence of osteoporosis in US 54% patients in US over the age of 50 years have
1/5 Medicare patients die within 12 months with a new osteoporotic fracture
osteoporosis or osteopenia
AACE screening criteria:
o All postmenopausal >50 years—can use FRAX when available to determine
fracture risk
o All women >65 years need BMD testing
o Postmenopaual women with history of fracture without major trauma or high risk
WHO diagnostic criteria for osteoporosis:
need BMD testing/DEXA
AACE diagnostic criteria for osteoporosis:
o T-Score -2/5 or below
o T-score -2.5 or below in L spine, femoral neck, total proximal femur or 1/3 radius
o Low trauma spine or hip fracture regardless of BMD
o T-score 1- -2.5 and fragility fracture of proximal humerus, pelvis or distal forearm
Evaluation for secondary causes of osteoporosis
or high FRAX 10 year prob for major osteo fracture >20%
o Most are disorders of calcium and PTH
o Hypercalciuria, high PTH, vitamin D deficiency, hyperthyroidism, Cushing’s,
Labs to order:
metabolism of calcium
o CBC, CMP including albumin, LFTs, phosphorus, 24 hr urine Ca, Na, Cr
o PTH
o Serum vitamin D 25 hydroxy
o TSH
o Screening tests for celiac disease
Nonpharmacologic management:
o CTx
o Calcium- 1200mg/day for women >51 or men >71
Pharmacologic therapies:
o Vitamin D 1000-2000IU/ day. Goal Vit D 30-50 ng/ml
o Antiresportive therapies
Bisphosphonates Denosumab
SERMs
Estrogen
Calcitonin
o PTH analogs
o Evenity (romosozumab)
Who needs pharmacologic therapy?
o T-score -2.5 or below in L spine, femoral neck, total proximal femur or 1/3 radius
o Low trauma spine or hip fracture regardless of BMD
o T-score 1- -2.5 and fragility fracture of proximal humerus, pelvis or distal forearm
or high FRAX 10 year probability for major osteoporotic fracture >20%
What is a “Very high fracture risk”? THESE ARE SOME EXAMPLES:
o Recent fractures withino Given as 2 subcutaneous injections totaling 210 mg monthly
o Black box warning: CI in patients with stroke/MI in the last 12 months
o FRAME trial 75% reduction in vertebral fracture in 24 months when compared
with placebo. All patients received denosumab after 12 months of either
romosozumab or placebo
Transitioning from denosumab
o ARCH trial 48% reduction in vertebral fracture
o Need to have a proper transition plan
o Rapid decrease in BMD with discontinuation after 2 to 8 years
o Can have fractures within 8-16 months
Switching to injectable therapies
o Can transition to alendronate or zoledronate
o Progression of bone loss or recurrent fractures
o Assess compliance
o Re-evaluation of secondary osteoporosis
o Switch to injectable if on oral agent
o If already on injectable change to abaloparatide, teriparatide or romosozumab
Common Supplements Use by Endocrinology Patients: Facts and Myths—Rashmi
Mullur, MD
Summarized by: Jaspreet Hehar, MD (Fellow, Henry Ford Hospital)
The Dietary Supplement Health and Education Act (DSHEA) passed in 1994 defines a “dietary
supplement” as any vitamin, mineral, herb/botanical, amino acid, or dietary substance used to
augment the diet. Under this act, supplement manufacturers do not need to receive FDA
approval before marketing, and there is no limit to the amount of vitamins or minerals that be
can put into a pill. As a result, there may be risks with herbal supplements. These supplements
may be adulterated, and have also been found to contain detectable lead, mercury, or arsenic
that exceed the standards for acceptable daily intake of toxic metals. The most adulterated
drugs are those used for weight loss, sexual enhancement, or bodybuilding.
Native American healers, traditional Chinese medicine and Ayurvedic medicine have used
herbal supplements for medicinal purposes for centuries. The WHO estimated that about 80% of
some Asian and African countries use herbal medicines, likely due to increased cost of
pharmaceuticals versus herbal medicines which can be grown for little or no cost. In the US,
supplement use is influenced by health care access, racism, trust in health care, chronic
disease, education and socioeconomic status. Data shows there is higher incidence of
supplement use in patients with chronic diseases. In terms of socioeconomic status, there is a
U-shaped curve with increased use of supplements in those with higher socioeconomic status
as well as in those with lower socioeconomic status.
Dietary supplements can be grouped into various categories:
1. Nutraceuticals: product isolated from food that is used for medicinal and therapeutic
purposes (eg. flax seed oil).
2. Micronutrients: chemical element or substance that is beneficial for normal growth (eg.
multivitamins, Vitamins A, D, E, K).3. Herbal: plant-based product used for therapeutic use.
4. Glandular: compound created from animal sources that contains biologically active
hormones (eg. phytoestrogens women take after menopause).
5. Adaptogen: a supplement that can augment the body’s response to stress. Can be
derived from plants or mushrooms and has activity along immune and hormonal
pathways.
Herbs can also be prepared in various ways:
1. Tea: can be made from fresh or dried herb. Infusions are aerial parts of the plant steeped
in hot water. Decoctions are the woody parts of plants and are simmered in water for
longer time period
2. Extracts or tinctures: liquid preparations of fresh or dried herb processed with a solvent,
which can be dried, sprayed, or powdered into capsules.
3. Essential oils: distilled from the whole plant. Large amount of plant material is required.
Volatile oils are used in aromatherapy. Dermal/direct contact oils are used in massage.
Most should never be used orally.
The approach to dietary supplements should begin with asking the patient to list all the
supplements they are taking and document these by class in the medical record. These
supplements can be reviewed using a natural medicine database or NCCIH herbal supplements
source. Use of supplements should be guided by the patient’s health, dietary habits,
medications, and laboratory data. The most common use of these supplements by patients is for
glycemic or complication control in those with diabetes, improvement in sexual function or libido,
and management of fatigue and stress. Examples of some of these supplements are discussed
below.
Berberine: ammonium salt/plant alkaloid found in roots, rhizomes, stems, and bark of several
plant species. There are several active metabolites that target multiple intracellular pathways
including those that target insulin resistance, inhibiting key enzymes including amylase and
alpha-glucosidase, modulating gut microbiota and affecting lipid metabolism. One gram of
berberine has been shown to be effective in lowering body weight, glucose, and lipids. Many
drugs are in development to improve oral bioavailability, efficacy, and reduce potential toxicity.
Can be associated with P450 drug interactions. As an alkaloid compound, also need to monitor
liver function tests.
Alpha lipoic acid (ALA): This is an organosulfur compound found in plants, animals, and
humans. Acts as cofactor for enzymatic reactions of oxidative metabolism. Dietary sources of
ALA include spinach, broccoli, yeast extract as well as organ meats. Its mechanism of action
includes reduction of oxidative stress, improvement in nerve blood flow, and in nerve conduction
velocity. Supplementation of ALA up to 1800mg daily is considered safe for long term use.
Common side effect is GI upset. ALA has been found to be effective in the treatment of diabetic
peripheral neuropathy.
Tribulus terrestis: Grows in the wild in dry climates and is considered an aggressive, invasive,
and noxious weed. Studies have shown it to suppress downstream effects of angiotensin II.
Clinically, it has been used to treat angina, erectile dysfunction, and hypogonadism. However,the data does not support the use of Tribulus in male infertility and hypogonadism, and it is
important to recognize that Tribulus supplements may be adulterated with pharmaceuticals. If
one has a patient taking this supplement, measure testosterone and DHT levels, ask why the
patient is taking it, and if there is benefit from it in their sexual desire symptoms. It is effective in
treatment of hypoactive sexual desire disorder in men and women. It is important that Tribulus is
not used with nitrates.
Rhodiola Rosea: This is a flowering biennial used in traditional medicine to manage stress,
fatigue, depression, altitude sickness, and exhaustion. It has been shown to lower peak cortisol
levels. For major depressive disorder (MDD), phase 2 trial has shown Rhodiola has been
effective for those with MDD and with fewer side effects compared to sertraline.
Ashwagandha: Also known as Indian ginseng. This is a plant in the nightshade family that has
been studied for its stress relieving effects. High doses of >600mg per day have not been
studied, and it can be associated with acute liver injury. Its mechanism of action includes
downstream effects on several pathways affecting anti-inflammatory markers, apoptotic and
anti-proliferative factors, as well as antioxidative factors. In 2 small clinical trials, it has been
shown to mildly reduce cortisol levels. It also impacts thyroid function tests in subclinical
hypothyroidism by increasing T3 and T4 and slightly lowering TSH.
In summary, Berberine can improve glycemic outcomes and may offer CV benefit but must be
used with caution due to herb interactions and liver injury. Alpha lipoic acid is helpful in
treatment of diabetic peripheral neuropathy and is generally well tolerated. Tribulus is effective
in treating hypoactive sexual desire disorder, however it is commonly adulterated so use with
caution. Rhodiola lowers cortisol levels and can improve symptoms of MDD with fewer side
effects. Ashwagandha lowers cortisol levels and affects other hormonal pathways as well, but
high doses have not been studied and it can be associated with liver injury.
Many patients feel like supplements help them. Have an open dialogue with patients and advise
them to stop supplements if there is any liver function test abnormality, concern for adulteration,
and/or drug-herb interactions. One can always refer the patient to the national center for
complementary and integrative health as a reference source.
Common Supplements Use by Endocrinology Patients: Facts and Myths—Rashmi
Mullur, MD
Summarized by: Olga Libova, DNP, post-graduate Family Nurse Practitioner student (SFSU
SON)
In the US, spending on nutrition supplements (“non-vitamin, non-mineral natural products”) was
$12.8 billion per year in 2012 and only continues to grow. Regulation of dietary supplements is
covered under a different set of regulations than those covering "conventional" foods and drug
products. Under the Dietary Supplement Health and Education Act of 1994 (DSHEA),
supplement manufacturers do not need to receive FDA approval before marketing dietary
supplements and there is no limit in the amount of vitamins that can be put into a pill. The herbal
and supplemental market has grown to include more than 29,000 products.In 2007, the FDA passed a Current Good Manufacturing Practices rule for dietary supplements (DS CGMP Rule). Potential issues with supplements include significant difference in contents and ingredients, contamination of herbs with heavy metals (arsenic, mercury, etc.), adulteration with pharmacological ingredients, especially in weight loss, sexual enhancement and body- building products. Herbs and other non-pharmacological products have been continuously used in most other countries as a part of comprehensive medical approach, with the most widely known being Traditional Chinese Medicine (TCM) in Chinese-speaking countries, Ayurveda in India, Homeopathy and naturopathy in Europe, particularly Germany, where traditional apothecaries have been providing care for generations. In the US, on the other hand, consumers often choose “natural” products themselves without the guidance of a practitioner. US consumers using supplements are more likely to suffer from a chronic condition and be either unable to afford pharmaceutical treatment due to lack of medical insurance or be quite affluent and use these products as a “supplement.” Indeed, consumers also often cite “Ownership of healthcare” as a reason to use supplements. The categories of supplements include nutraceuticals (derived from food), micronutrients (chemical elements or substances), herbal (derived from herbs), glandular (created from animal or sometimes plant source and containing one or more biologically active hormones), adaptogen (recently a separate category of plant/mushroom-based substances that are supposed to enhance body’s response to stress and often act along immune and hormonal pathways). Plant chemistry is much more complex than pharmaceuticals which often causes an “entourage effect” (a synergetic effect most commonly discussed in relation to effect of cannabis plant being more comprehensive than effect of its components separately). The way the plant is prepared affects how it gets absorbed. Preparations include teas (infusions and decoctions), tinctures or extracts (prepared as liquid and then dried) or oils (most oils should never be used orally). It is important to ask the patient about their use of supplements, including product, preparation, dose, what are they taking it for, include it in patient’s medical record, review the safety of the product and possible interactions in the databases (see resources below) and discuss the use with the patient guided by their overall health, dietary habits, medications, labs, wellness goals. Most common reasons that patients are using supplements in Dr. Mullur’s practice are: Glucose control and complications (pain) control in diabetes, to improve sexual function/libido, stress/fatigue management. Products: Berberine is an ammonium salt found in yellow root, goldenseal, barberry. It has been shown to have poor gut absorption and fast metabolism, but several active metabolites that target different pathways involved in insulin resistance, gut flora, lipid metabolism. It may cause herb/drug interaction through P450 and has an effect on liver function tests. Alpha Lipoic acid (ALA) is found in many plant and animal based foods but is not readily available in food form. It is used for improving the symptoms of diabetic peripheral neuropathy.
You can also read
