I am often asked about hair loss in WLS patients, so I did a little research and found an article from the Obesity Action Coalition written by Jacqueline Jacques that describes how hair grows, the risk factors and treatments for hair loss.

I am including her conclusion and will provide a brief summary of the article.

Conclusion
Hair loss can be distressing to bariatric surgery patients and many will try nutrition themselves to see if they can prevent it. Unfortunately, there is little evidence that early hair loss is preventable because it is mostly likely caused by surgery and rapid weight-loss.

Later hair loss, however, can be indicative of a nutritional problem, especially iron deficiency, and may be a clinically useful sign. Educating patients about the potential for hair loss and possible underlying causes can help them to make informed choices and avoid wasting money on gimmicks that may have little real value.

Summary:
At any given time most of our hair is in a 'growth phase', but a small percentage is in a 'resting phase'. A number of stressors can cause a greater percentage of our hair to move into a resting phase and WLS patients are at particular risk because we have all had major surgery and experience rapid weight loss which are among the stressors that can impact having a larger percentage of our hair being in the resting phase. Also, if we are experiencing low values of ferritin, zinc or protein or have had more rapid than expected weight loss we may be at greater risk of hair loss.

While some think that supplementing with Biotin, topically or ingesting it; studies have not shown it to be effective in either stopping hair loss or improving regrowth.

 

I found an article on Metabolic Bone Disease from the Journal of Obesity. I am including the summary and highlighting the areas that I think are most important. If you want to read the complete article, click this link.

Bariatric surgery has proven to be an effective and life-saving measure that provides sustainable weight loss but it is not without risk of complications, to include metabolic bone disease (MBD).

There is a causal, multifactorial relationship between bariatric surgery and MBD and for that reason MBD remains an ever-present risk in bariatric surgery patients.  Patients presenting for bariatric surgery should be evaluated for MBD and receive appropriate presurgical interventions. Postsurgically, the importance of consuming adequate protein and the correct combination of vitamins and minerals cannot be overstated, remembering that no bariatric surgical procedure is risk-free when it comes to the development of metabolic bone disease.

As clinicians, we cannot assume that our morbidly obese patients are well nourished or that they have normal bone quality.  Dual-energy X-ray absorptiometry can be used to help assess bone status in the morbidly obese, however if the DXA table limitations prevent imaging the hips and spine, the nondominant forearm is a validated option for quantifying bone mineral density.  

Not all abnormal DXA results represent primary osteoporosis and in fact, in the bariatric population, secondary bone disease is the norm and when the diagnosis has been confirmed, treating the underlying cause of the secondary disease must take precedent.  DXA Z-scores, if abnormally low, suggest the presence of secondary MBD, however it is important to remember that secondary disease can be present even in the presence of normal scores.  Clues such as proximal weakness, a history of renal oxalate stones, chronic steatorrhea, and undersupplementation should serve to alert the clinician to the possible presence of metabolic bone disease.

In addition to the AACE/TOS/ASMBS guidelines, a baseline and one year postoperative DXAs are recommended. The use of calcium citrate and cholecalciferol (vitamin D3) are the recommended forms of these supplements, and in order to achieve and maintain normal serum levels, very high doses are often required in the bariatric postoperative patient.

Caution is advised when considering the use of certain medications to treat common problems in this patient population.  Cholestyramine or other bile acid sequestrants used to control diarrhea in this patient population increase the risk of exacerbating vitamin D malabsorption and osteomalacia, and may increase the risk of bowel obstruction. The use of bisphosphonates for presumed osteoporosis carries the risk of life-threatening hypocalcemia; efficacy has not been well established in this population, and the risk for ulceration from oral preparations at the surgical anastamosis has yet to be delineated.

Finally, there is emerging evidence that bariatric osteomalacia is a unique and increasingly common phenomenon in bariatric surgery patients that can have a subtle clinical presentation but potentially devastating consequences if left unrecognized.  Investigations into the underlying mechanism of the disease, the response to aggressive repletion, and effective preventive strategies are ongoing.  The treatment regimen at this point in time includes the use of cholecalciferol and calcium citrate with frequent monitoring and dose adjustments to attain and maintain normal lab parameters.

I am a little over 3.5 years post RNY and  I had my labs run again. While most of the news was good news, it did show that I'm not absorbing as much D as I need so I got another Rx for 8 weekly doses of 50K of D3. We'll retest after this course and see how it's going. We're also checking with my insurance to see about starting a regimen of ReClast or another injectable medication to help reverse the osteoporosis I've developed and hopefully get me back to the land of osteopinia if not back on solid ground. I have really been worrying that I had compromised my health with my decision to have RNY and have been beating myself up about it. My PCP said that I have to remember that while my RNY is likely a contributing factor in my fight with osteoporosis, that the meds I take for my depression, my family history and the fact that I hit menopause at the same time I had my RNY are all likely significant factors in my osteoporosis. He said that he felt that my osteoporosis is mild at this time and that he thinks we can reverse it with a combination of managing my supplementation, exercise, and alternating medications for osteoporosis with estrogen therapy. (We'll do a year of Reclast and when we take off a year to give my bones and body a break fromt he Reclast, we'll put me on estrogen therapy to try to maintain the bone stores, then switch back to the Reclast the following year, and so on...) He said that the relative trade-offs that my labs showed in healthy glucose, cholesteral, lipids, etc. are a testament to my good overall general health and that he thought that everything we do has tradeoffs. That said, he thinks my decision to have my WLS have served me well. That was comforting.

I visited the orthopedic Dr to address my back and the pain associated with the compression fractures I have in my back. My PCP originally Rx'd Hydrocodone and while they did seem to take the edge off of the pain, they also seemed to wear off very quickly and then I was hurt for several hours without any relief. My PCP then Rx'd Oxycontin which is a longer acting medication. Again, this seemed to help some, but also seemed to wear off long before the next dose was due. On top of that, I'm not a big fan of taking medications that are addictive, so to be honest I wasn't taking them quite as much as I should. This was leading to pain and not being able to sleep very well. The PCP had orginally Rx'd the pain management medications in response to my fractured wrist. When I went back to see him because my back was hurting, he Xray'd my back uncovering the compression fractures and suggested that I see a colleague that specializes in treating back injuries and managing the pain associated with them. She prescribed a Fentanyl patch. The patches last for 72 hours each, but it takes a while for the medication to build up in your system, so I'm just now beginning to 'enjoy' the pain relief. It's the first time in more than a month where my pain level has been below a 2 or 3 on the pain scale. I know that may not seem like a big deal, but it's been between a 2 and a 7 for over a month. Until last night, I hadn't slept for more than 3 to 5 hours a night and sleep deprivation can get mean after a while so I'm really grateful for the break. I'll be using the patch for the next month. After that, we'll see what happens. I'm hoping I won't be hurting anymore and won't need anything. I'm supposed to abstain from exercise until further notice. When I can exercise again, I'll work with a physical therapist to make sure I don't hurt myself again. I want to improve my balance, strength and aerobic endurance in hopes that it will improve my overall and skeletal health.

I'm working on trying to make sure that I not only get in my requisite calcium citrate and vitamin D, but also that I am eating a diet rich in vitamins and minerals such as calcium, magnesium, iron, etc...