Sweet potatoes are a bone-building super food for supporting your bones in fall and winter with alkalizing vitamins and minerals. But there’s an asterisk here, and it’s about how you prepare these root vegetables.
Unfortunately, many of the most common sweet potato recipes emphasize added sugars — brown sugar, maple syrup, or molasses used to “glaze” roasted sweet potato slices or added to mashed sweet potato to make it sweeter. (Some of my readers may be familiar with a holiday dish of mashed sweet potatoes covered in, of all things, marshmallows).
These acid-forming sugars, even if they’re natural (like maple syrup), tip the scales away from sweet potatoes’ inherent alkaline-forming state. At best, such recipes provide a neutral input that neither harms nor benefits your overall pH — and at worst, the negatives from the added sugars overwhelm the positives that the sweet potato brings to the table.
Sweet potato recipes that skip the sugar
Fortunately, there are a lot of recipes available that feature roasted sweet potatoes in warm salads (a great winter dish) that avoid adding sweeteners and focus instead on balancing the potato’s naturally sweet flavor with savory spices. For a hearty cold weather lunch, try this Warm Quinoa, Sweet Potato and Kale recipe.
Another recipe that I’ve found particularly intriguing is a dish that features roasted sweet potatoes, cranberries, almonds, and scallions in a mango chutney vinaigrette. It is a flavorful — and highly alkalizing — addition to your Thanksgiving or holiday meal menu. Find my take on this recipe below. Let me know how you like it!
Sweet potatoes are an alkalizing food we can all be thankful for. I encourage you to explore the many options you have for warm, savory sweet potato salads as a way to enjoy this healthy root and obtain its bone-supporting nutrients for your bones this holiday season and throughout the winter months ahead.
Roasted Sweet Potato Salad With Chutney Vinaigrette Recipe
Adapted from SeriousEats.com
3 sweet potatoes
3 Tbsp olive oil
1 tsp salt
1 tsp cumin
1 tsp ground ginger
3 Tbsp balsamic vinegar
2 Tbsp mango chutney
1 Tbsp Dijon mustard
1 tsp minced garlic clove
2 Tbsp olive oil
1/2 cup dried cranberries
1 cup chopped scallions
1/2 cup sliced almonds, toasted
1. Preheat oven to 425°F. Line a large baking tray with aluminum foil.
2. Peel and cut sweet potatoes into 1-inch chunks.
3. Toss sweet potatoes with olive oil, salt, cumin, and ginger. Spread on baking sheet. Roast until potatoes are tender, about 30 minutes. Stir occasionally for even roasting.
4. Combine vinegar, chutney, mustard, garlic, and olive oil in a bowl and whisk to combine into dressing.
5. Remove potatoes from oven and allow to cool slightly (about 10 minutes).
6. Toss potatoes with the dressing mixture.
7. Transfer to serving platter and scatter almonds over top. Serve warm or room temperature.
I recently recorded a Facebook Live video critiquing a new study that suggested vitamin D does not prevent bone fracture. This study was published in The Lancet in October 2018 and was clearly flawed in many ways. For those of you who did not catch my video commentary on the shortcomings of this study, I summarize them here.
Not all studies are created equal
I’ve been looking at the research on vitamin D for almost 30 years. It’s been clear for quite some time that you can reduce fracture risk with vitamin D if you obtain the therapeutic level of 32 ng/mL in your blood. So why would the new study claim that vitamin D doesn’t work to lower fracture risk?
To put it simply, the new study used a lot of vitamin D data that just wasn’t very good to start with. As a meta-analysis, it mined data from 80 studies on vitamin D from the past 20 to 30 years. But the problem is that most of these studies were flawed in the following ways:
They were mostly evaluating low doses of vitamin D (400–800 IU) that we know to be too low to affect fracture risk.
Many of them were too small and too short in duration to really assess the effectiveness of an intervention with vitamin D.
To be valuable, the study must document not only how much the participants took, but also whether they reached the therapeutic level. The vast majority of the studies didn’t report what blood level their participants reached—so none of them can say for sure that their participants had adequate vitamin D levels, particularly since few of them assessed the starting blood levels.
In those studies that did give higher doses of vitamin D, most of the time it was supplied in a single bolus of 100,000–300,000 units — which has been shown to be ineffective. To be most effective, the vitamin D dose should be given daily and it should always be given in the form of a natural vitamin D3 (cholecalciferol), not vitamin D2 (ergocalciferol).
The standard treatment for vitamin D deficiency uses 7,000 IU of vitamin D daily for 8 weeks, followed by testing of the new vitamin D level. Then the appropriate, long-term dose of vitamin D is determined. This is a dose that would provide at least a 32 ng/mL blood level of vitamin D, the minimum needed for health, with the goal of reaching an ideal range from 50–60 ng/mL.
Once vitamin D deficiency has been corrected, most individuals require 3000–4000 IU (or more) supplemental vitamin D daily to maintain an optimum blood level.
When you look at the data the study used, it’s pretty clear that this recent metanalysis is serious flawed, and that the author’s conclusion that vitamin D is of no use in fracture prevention is both irresponsible and harmful.
So don’t be fooled — the value of vitamin D, established over many years of good research, is no different in 2018 than it was in 2008, when I first published my research review article on the subject.
Bolland MJ, Grey A, Avenell A. Effects of vitamin D supplementation on musculoskeletal health: a systematic review, meta-analysis, and trial sequential analysis. Lancet Diabetes Endocrinol. Published online October 04, 2018. DOI:https://doi.org/10.1016/S2213-8587(18)30265-1.
Brown SE. Vitamin D and fracture reduction: An evaluation of the existing research. Altern Med Rev. 2008;13(1): 21-33.
Another new bone drug — Tymlos (abaloparatide) — recently hit the market, approved by the FDA for treating osteoporosis in postmenopausal women.
As always when we get a new entry into this ever-more-crowded market, I wanted to see how Tymlos works in the body and what downsides could be lurking behind all the hype. Is Tymlos safe? I wish I had a new and different message for you about Tymlos. Believe me, it would be nice to be able to say, for once, that the newest product on the bone drug market really is good for bones — and safe for those who take it. Unfortunately, I can’t say this.
Tymlos — how does it work?
Tymlos, like Forteo before it, works by imitating a natural bone-building process in the body to increase the patient’s bone density. It’s similar to Forteo in that it focuses on the parathyroid hormone (PTH) pathway, except that while Forteo mimics PTH itself, Tymlos mimics a peptide called human parathyroid hormone-related protein (PTHrP) — but the end result is the same: stimulation of the PTH pathway to increase osteoblast activity, with the goal of building denser bone. If Tymlos works along similar lines as Forteo, then it stands to reason that it’s going to have similar drawbacks — and it does.
The side effects of Tymlos — a deeper look
Like Forteo, Tymlos comes with a warning about osteosarcoma, a rare bone cancer. The warning is based on animal studies that have shown increased rates of this cancer in animals dosed with abaloparatide (Tymlos). Rather ironically, one study cheerfully noted that their results “suggest no increased risk of osteosarcoma would be expected in patients treated with [Tymlos]” in comparison to Forteo — which itself offers a greater-than-normal risk of osteosarcoma, so that’s not much of a recommendation.
Another adverse effect in the warning list is orthostatic hypotension — that is, low blood pressure upon standing, which could lead to fainting or falls (not something you want in a person at high risk of fracture!). High blood or urine calcium levels (the latter in association with kidney stones) are also concerning side effects.
Further, the effects of this drug on the immune system is really unexplored and only lightly touched upon in the safety trials. Half of the individuals using the new drug developed antibodies to the drug which in some cases lead to cross-reactivity, and in all cases squantered precious immune system focus and energy.
It’s also notable that a large, double-blind clinical trial with 2,463 women (age 49–86) comparing Tymlos directly to Forteo and placebo, Tymlos significantly outstripped both the placebo group and the Forteo group in terms of participants who had to stop treatment due to side effects such as nausea, dizziness, headache, and palpitations; where the Forteo group had about an 0.7% absolute increase in such side effects over the placebo group (a relative increase of 11%), the Tymlos group experienced a whopping 3.8% increase (a 61% relative increase) in these effects over the placebo group.
How much does Tymlos really reduce fracture?
I bring up the “absolute” vs. “relative” increases in side effects for a reason: The 43% nonvertebral fracture risk reduction in Tymlos-treated patients sounds fantastic until you realize it’s relative risk, not absolute risk. In absolute terms, the placebo group had 2% more nonvertebral fractures than the Tymlos group — meaning for every 100 women who took this drug and dealt with its side effects, 2 were spared a nonvertebral fracture who would’ve had one if they’d done nothing. And how about vertebral fractures? This new drug was only slight more successful at reducing vertebral fractures — reporting a absolute reduction of 3.64%. One hundred women have to be treated for 3.64 spinal fractures to be prevented. (Given the exorbitant cost of this drug, that’s not such a great return on investment!)
Ultimately, this drug has the same problems most of the others have — it hijacks the body’s natural processes to force a result without consideration for the unintended consequences. Which begs the question: Why not work with the body to strengthen bones the way nature intended?
Hattersley G, Attalla B, Varela A, Smith SY. Comparison of osteosarcoma incidence between abaloparatide (BA058) and PTH (1–34) in long term rat studies. Bone Abstracts (2014) 3 PP302 | DOI: 10.1530/boneabs.3.PP302
Miller PD, Hattersley G, Riis BJ, et al; for the ACTIVE Study Investigators. Effect of Abaloparatide vs Placebo on New Vertebral Fractures in Postmenopausal Women With Osteoporosis: A Randomized Clinical Trial. JAMA. 2016;316(7):722-733. doi:10.1001/jama.2016.11136
Tymlos Prescribing Information. Radius Pharmaceuticals. Web. http://radiuspharm.com/wp-content/uploads/tymlos/tymlos-prescribing-information.pdf